Domestic Cat Hepatitis B Virus

While Domestic Cat Hepatitis B Virus is more properly called Domestic Cat Hepadnavirus, we will keep using the more accepted naming system.
A novel Hepatitis B Virus was discovered in a domestic cat from Australia[1]. In 2016, a seven year-old male-neutered domestic shorthair cat was presented for vomiting and weight loss. Diagnosed with Feline Immunodeficiency Virus (FIV), the cat was eventually euthanized.

To identify potential viral pathogens infecting domestic cats scientists performed high-throughput transcriptome sequencing of tissues from cats infected with Feline Immunodeficiency Virus (FIV).

During that investigation several cats, that had previously died as a result of FIV, also seemed infected with a virus. The virus itself was elusive and it showed only 73–94% amino acid identity with known Hepatitis B viruses. This suggested the presence of a novel virus that was divergent from currently known Hepatitis B viruses. Such a large genetic distance merits assignment of a new species within the genus Orthohepadnavirus, which was tentatively named Domestic Cat Hepadnavirus or Domestic Cat Hepatitis B Virus.

Further research revealed that it exhibited no close phylogenetic relationship to any other known Hepatitis B virusses.

[1] Aghazadeh et al: A Novel Hepadnavirus Identified in an Immunocompromised Domestic Cat in Australia in Virusses – 2018. See here.

Immune system does not recover despite cured Hepatitis C Virus infection

Changes to the immune system remain many years after a Hepatitis C Virus infection heals, a new study shows[1]. The findings increases understanding about chronic infection and the way it regulates and impacts composition of the immune system.

Infection with Hepatitis C Virus turns almost always chronic and poses a major health problem around the world. The infection can lead to cirrhosis and cancer of the liver when the immune system fails to fight the virus. Eventually the immune system becomes exhausted. Since a couple of years, however, most patients with Hepatitis C Virus can now be cured in a matter of a few weeks with revolutionary new medications.

The study included 40 patients with chronic Hepatitis C Virus infection whom researchers followed before, during and after treatment with these new medications to investigate impact on the composition and diversity of the immune system. Diversity is vital to the ability of the immune system to fight infections. Of particular importance are natural killer cells, a type of white blood cells. The researchers used flow cytometry and a new measurement method to derive the composition of the immune system, as well as the appearance of natural killer cells and their function in the blood.

“Researchers in the field previously focused on analysing individual components but were unable to draw any comprehensive conclusions,” says Niklas Björkström, who led the study. “The immune system is extraordinarily complex, incorporating a large number of interacting parts. We adapted new methods in order to assess and analyse that complexity in a fresh manner.”

The results showed that the overall composition of the immune system was affected by the chronic infection, with significantly reduced diversity among the natural killer cells. Many of the changes remained long after the virus had been eliminated by means of medication. Researchers have not yet determined the long-term implications but are currently exploring whether patients have a harder time fighting future infection.

Strunz et al: Chronic hepatitis C virus infection irreversibly impacts human NK cell repertoire diversity in Nature Communications - 2018

Hepatitis B Virus and Genghis Khan

The man who conquered almost the entire known world was originally called Temujin. It means 'of iron' in Mongolian and is derived ultimately from the old Turkish word temür ('iron'). We know him Genghis Khan(c. 1162-1227), the Mongol warrior who started life as a nomad in Mongolia. Later, his armies swept across the Asian steppes, conquering all they encountered. Only his timely death as a frail and sickly 65-year old Genghis Khan could arrest the hordes from reaching Europe.
Now, scientists found evidence that Mongol warriors from the steppe carried an early form of Hepatitis B Virus. Sequencing 304 genomes from the skeletons of people who lived on the steppe during the Iron and Bronze Ages (from about 2500 BC until 1200 AD), they found that twenty-five of the samples had DNA from Hepatitis B Virus in their bones[1].

That means that Hepatitis B Virus on the ancient steppes may have been as prevalent as it is in some of the most heavily impacted areas of the world today.
What the researchers found was that Hepatitis B Virus was circulating on the Eurasian steppes for thousands of years. One of the stains found is now extinct, having apparently faded out of existence sometime in the last 4,500 years. And one of the nine major genotypes circulating today appears to be the product of an ancient recombination between two strains of the Hepatitis B Virus.
[Novel genotypes A, B, C, D, E, F, G, H]
[Genotypes of Bronze Age and Iron Age]
Most of the genetic diversity in Hepatitis B viruses today probably arose sometime between 25,000 and 13,400 years ago, when the genetic lineages of Old World Hepatitis B strains and New World Hepatitis B strains split.

One modern strain, genotype A, was previously thought to have emerged in Africa and spread to the Americas and India within the last few centuries via the slave trade. But the researchers found some ancestral strains of type A in people living on the steppe as early as 4,300 years ago: some from the Sintasha culture in what is now southwest Russia, and one in a person from the Scythian culture in what is now Hungary.

That, suggests that it's the other way around, that it came from Europe, but it was introduced to South Asian populations historically recently.

[1] Mühlemann et al: Ancient hepatitis B viruses from the Bronze Age to the Medieval period in Nature – 2018

Stone Age and Medieval Hepatitis B Virus decoded

A team of researchers not only recovered ancient viral DNA from skeletons but also reconstructed the genomes of three strains of Hepatitis B Virus.
[Skeletal remains of HBV positive individual from the Stone Age site of Karsdorf (Germany). The individual was a male who died ataround 25-30 years. – Credit: Nicole Nicklisch]

For this study, the researchers analyzed samples from the teeth of 53 skeletons excavated from Neolithic and medieval sites in Germany[1]. The remains dated from around 5000 BC to 1200 AD. The researchers screened all samples for viral pathogens and detected ancient Hepatitis B Virus in three of the individuals. Full Hepatitis B Virus genomes were recovered from these samples, two of which were from the Neolithic period, dating to about 7000 and 5000 years ago, and one from the medieval period[2]. The Neolithic genomes represent the by far oldest virus genomes reconstructed to date.

Interestingly, the ancient virus genomes appear to represent distinct lineages that have no close relatives today and possibly went extinct. The two Neolithic genomes, although recovered from individuals that lived 2000 years apart, were relatively similar to each other in comparison with modern strains, and were in fact more closely related to modern strains of Hepatitis B Virus found in Chimpanzees and Gorillas. In contrast, the medieval Hepatitis B Virus genome is more similar to modern strains, but still represents a separate lineage. This is the case even when it is compared to two previously published Hepatitis B Virus genomes recovered from mummies dating to the 16th century. The Hepatitis B Virus strains found in these mummies are closely related to modern strains, suggesting a surprising lack of change in the virus over the last 500 years.
These findings point to a complicated history for the virus, which may have involved multiple cross-species transmission events.

[1] Ben Krause-Kyora et al: Neolithic and Medieval virus genomes reveal complex evolution of Hepatitis B in eLife – 2018
[2] Patterson Ross et al: The paradox of HBV evolution as revealed from a 16th century mummy in PloS Pathogens - 2018

Hepatitis A Virus in Molluscs

Hepatitis A Virus is primarily spread when an uninfected and unvaccinated person ingests food or water that is contaminated with the faeces of an infected person. The disease is closely associated with unsafe water or food, inadequate sanitation and poor personal hygiene. When you are infected with Hepatitis A virus, you might experience some rather unpleasant symptoms. These include fever, malaise, loss of appetite, diarrhoea, nausea, abdominal discomfort, dark-coloured urine and jaundice (a yellowing of the skin and whites of the eyes). Not everyone who is infected will have all of the symptoms.
One of the places you might venture into quite frequently when you have diarrhoea is the toilet. In several countries faeces still is led untreated into the sea. So, the question is therefore, is Hepatitis A Virus able to infect (edible) molluscs.

Scientists studied of a total of 352 samples, including four bivalve mollusc species, the Mediterranean mussel (Mytilus galloprovincialis), the European razor clam (Solen vagina), the striped venus clam (Venus gallina) and the abrupt wedge shell (Donax trunculus). Hepatitis A Virus was detected in 77 samples[1]. All of these molluscs are consumed in the Mediterranean.

If you like to eat your molluscs raw, you should be aware that you could become infected with Hepatitis A Virus.

[1] Suffredini et al: Occurrence and Trend of Hepatitis A Virus in Bivalve Molluscs Production Areas Following a Contamination Event in Food and Environmental Virology - 2017

Hepatitis E Virus in Namibia

During the week ending on 13 October 2017, the first identified case was admitted to a public hospital in Windhoek district, with signs and symptoms of hepatitis E. During the week ending on 8 January 2018, a total of 237 probable and confirmed cases have been seen at various health facilities in Windhoek district with the same signs and symptoms. All suspected patients tested negative for hepatitis A, B, and C. A total of 41 of the 237 cases were sent for further testing, and on 8 January 2018, the results showed 21 were IgM positive for hepatitis E. On 19 November 2017, there was one confirmed deceased case, a 26 year-old female. Four days prior to her death she had delivered a baby. The status of the baby is unknown. The majority of the cases were from Windhoek district, Khomas region.
[The number of patients seen with acute clinical jaundice in Windhoek district by week, from September 2017 to 8 January 2018 (n = 237)]

Although infections with Hepatitis A, B and C are common in Namibia, Hepatitis E is rarely diagnosed in the country. As a result, the country has limited capacity for hepatitis E laboratory diagnosis. Additionally, the majority of hepatitis E cases have been reported from informal settlements within the capital district, Windhoek, where living conditions are poor. These areas are overcrowded, have limited access to safe drinking water, sanitation and hygiene.

Moreover, the holiday season will likely increase the movement of people within the country. All of these could be major contributing factors to this outbreak.

Additionally, during the rainy season, people often use rainwater or other surface water for drinking and domestic uses. This likely increases the risk of hepatitis E infection. Therefore, the above-mentioned factors might lead to the propagation of the cases from this area to other informal settlements and its distribution to other towns or districts, with similar poor environmental health conditions. Thus, the overall risk is assessed as high at the national level and low at regional and global levels.

Hepatitis B Virus in 16thC Mummified Child

Little is known about the evolutionary history and origin of Hepatitis B Virus. Recent research confirms the idea that Hepatitis B Virus has existed in humans for centuries[1]. Scientists extracted genomic data extracted from the mummified remains of a child buried in the Basilica of Saint Domenico Maggiore in Naples (Italy).
Previous scientific analysis of the 16th century (radiocarbon dating is AD1569±60) remains suggested the child was infected with Variola virus, or smallpox[2]. In fact, this was the oldest evidence for the presence of smallpox in Medieval remains and a critical time stamp for its origins.

Using advanced sequencing techniques, researchers now suggest otherwise: the child was actually infected with Hepatitis B Virus. Interestingly, children infected with Hepatitis B Virus infections can develop a facial rash, known as Gianotti-Crosti syndrome. This may have been misidentified as smallpox and illustrates the difficulties of identifying infectious disease in the past.
“The data emphasizes the importance of molecular approaches to help identify the presence of key pathogens in the past, enabling us to better constrain the time they may have infected humans,” explains Hendrik Poinar, an evolutionary geneticist. “The more we understand about the behaviour of past pandemics and outbreaks, the greater our understanding of how modern pathogens might work and spread, and this information will ultimately help in their control,” says Poinar.

Using small tissue samples of skin and bone, scientists were able to tease out tiny fragments of DNA and then stitch together pieces of genetic information to create a much more complete picture.

While viruses often evolve very rapidly - sometimes in just days - researchers suggest that this ancient strain of Hepatitis B Virus has changed little over the last 450 years and that the evolution of this virus is complex.

The team found a close relationship between the ancient and modern strains of Hepatitis B Virus, but both are missing what is known as temporal structure. In other words, there is no measurable rate of evolution throughout the 450-year period which separates the mummy sample from modern samples.

[1] Patterson Ross et al: The paradox of HBV evolution as revealed from a 16th century mummy in PloS Pathogens - 2018
[2] Marennikova et al: Smallpox diagnosed 400 years later: results of skin lesions examination of 16th century Italian mummy in Journal of Hygiene, Epidemiology, Microbiology and Immunology - 1990

Hepatitis C Virus and Opioid Abuse

New research suggests that the recent steep increase in cases of acute Hepatitis C Virus infection is associated with increases in opioid injection[1]. Across the nation, researchers found substantial, simultaneous increases in acute Hepatitis C (+133 percent) and admissions for opioid injection (+93 percent) from 2004 to 2014. These increases were seen at not only the national level, but also when data were analysed by state, by age, by race and ethnicity. Taken together, the findings point to a close relationship between the two troubling trends.

For an analyses about the opioid crisis, see here and here.
About 75 to 85 percent of newly infected people develop a chronic Hepatitis C Virus infection. As there are few noticeable symptoms, many people are unaware of their infection until serious liver problems or other health issues arise. Hepatitis C is therefore a potentially deadly and often invisible result of America’s opioid crisis.

The new analysis builds upon earlier research identifying a similar regional trend in four Appalachian states that faced increasing rates of new Hepatitis C Virus infection[2].

Hepatitis C is spread through infected blood, which can contain high levels of the virus in a single drop. This, combined with needle and injection equipment sharing behaviours among some people who inject drugs, is fuelling infections among younger Americans.

Until recently, Hepatitis C primarily affected older generations, but as the opioid crisis worsened, the virus gained a foothold among younger Americans. Most of the 3.5 million people in the United States already living with Hepatitis C are born between 1945 and 1965, but the greatest increases in new infections are being seen in young people. And as infections increase among young women, so has the rate of Hepatitis C among pregnant women, placing a new generation at risk.

[1] Zibbell et al: Increases in Acute Hepatitis C Virus Infection Related to a Growing Opioid Epidemic and Associated Injection Drug Use, United States, 2004 to 2014 in American Journal of Public Health – 2017
[2] Zibbell et al: Increases in Hepatitis C Virus Infection Related to Injection Drug Use Among Persons Aged ≤30 Years — Kentucky, Tennessee, Virginia, and West Virginia, 2006–2012 in Morbidity and Mortality Weekly Report (MMWR) – 2015. See here.

New Hepatitis B-like virus family discovered: Metahepadnaviruses

The family Hepadnaviridae contains Hepatitis B viruses that are enveloped viruses with reverse-transcribed DNA genomes.

However, recently scientists reported the discovery of a new family of fish viruses, designated Metahepadnaviruses, which lack one of the four Open Reading Frames, the ORF X, compared to Hepadnaviriruses.
The ORF X encodes a 16.5-kd protein (HBxAg) with multiple functions, including signal transduction, transcriptional activation, DNA-repair and inhibition of protein degradation. The mechanism of this activity and the biologic function of HBxAg in the viral life-cycle remain largely unknown. However, it is well established that HBxAg is necessary for productive Hepattis B infection in vivo and may contribute to the oncogenic potential of Hepattis B viruses[1].

Otherwise these Metahepadnaviruses exhibit key characteristics of Hepatitis B viruses, including genome replication via protein-primed reverse-transcription and utilization of structurally related capsids[2].

The very first of these Metahepadnaviruses is the Tetra Metahepadnavirus (TMDV) of the Mexican tetra (Astyanax mexicanus). Collectors covet this species because it consists of distinct two subspecies: a 'normal' and a blind version.

Thousands of years ago, a population of Mexican tetras in northeastern Mexico swam (or was swept) from its hospitable river home into underwater caves and became trapped. Facing a dramatically different environment of near total darkness and hardly any food, the fish had to adapt very fast. Among other changes, these 'cavefish' swiftly (in evolutionary terms, within just a few thousand years) lost their pigmentation and their eyes. Regressive evolution is the correct term[3].

[1] Liang: Hepatitis B: The Virus and Disease in Hepatology – 2010
[2] Lauber et al: Deciphering the Origin and Evolution of Hepatitis B Viruses by Means of a Family of Non-enveloped Fish Viruses in Cell Host & Microbe – 2017
[3] Protas et al: Regressive Evolution in the Mexican Cave Tetra, Astyanax mexicanus in Current Biology - 2008 

New Hepatitis B-like virus family discovered: Nackednaviruses

The family Hepadnaviridae contains Hepatitis B viruses that are enveloped viruses with reverse-transcribed DNA genomes.

However, recently scientists reported the discovery of a diversified family of fish viruses, designated Nackednaviruses, which lack the envelope protein gene, but otherwise exhibit key characteristics of Hepatitis B viruses, including genome replication via protein-primed reverse-transcription and utilization of structurally related capsids[1].
Phylogenetic reconstruction indicates that these two virus families, Hepadnaviridae and Nackednaviruses, separated more than 400 million years ago, even before the rise of tetrapods. Therefore, Hepatitis B viruses are of ancient origin, descending from non-enveloped progenitors in fishes.

Their envelope protein gene emerged de novo, leading to a major transition in viral lifestyle, followed by co-evolution with their hosts over geologic eras.

The scientists identified Hepatitis B-related viruses by homology searching in public sequence databases at the National Center for Biotechnology Information (NCBI). What they found were three new Hepatitis B-like viruses: African Cichlid Nackednavirus (ACNDV), Rockfish Nackednavirus (RNDV) and Sockeye Salmon Nackednavirus (SSNDV).

[1] Lauber et al: Deciphering the Origin and Evolution of Hepatitis B Viruses by Means of a Family of Non-enveloped Fish Viruses in Cell Host & Microbe – 2017. See here.

Chimpanzees and an Anthrax variant

In 2001, while studying chimpanzees in the Taï National Park in Ivory Coast, Fabian Leendertz watched an alpha male named Leo vomit, climb up on a low branch, then topple over and die. Leendertz thought the chimps had died of the familiar form of anthrax, caused by Bacillus anthracis[1].
Five years later, Leendertz and his team showed that what killed the chimps was an unusual form of anthrax[2]. Now, scientists present evidence that the microbe causing it, Bacillus cereus biovar anthracis, plays a huge role in the ecology of the rainforest, apparently causing a large proportion of all mammalian deaths[3].

The Taï strain has acquired two plasmids, pXO1 and pXO2, possibly from Bacillus anthracis, encoding most of the genes that make anthrax such a formidable killer[4].

Leendertz and his team examined samples from bones and carcasses from at least 20 different species, collected in the forest. They detected the pathogen in 81 of 204 carcasses and 26 of 75 bones. In addition to chimps, six monkey species, duikers, mongooses and a porcupine died of the disease. It appears to be responsible for about 40% of observed wildlife deaths. The killer strain is not limited to the Taï forest. Leendertz and others have linked wildlife deaths to Bacillus cereus in other Central African countries.
[Bacillus cereus]
Animals contract Bacillus anthracis when they inhale or swallow hardy spores released into the soil by cadavers. But Bacillus cereus in Taï may have a very different ecology and epidemiology. The researchers are looking at other possible sources. One candidate is carrion flies. Leendertz’s team found traces of Bacillus cereus DNA in 17 flies. If they help spread the disease, that might explain how some monkey species that only live in trees become infected.

In humans, Bacillus cereus is responsible for foodborne illnesses, causing severe nausea, vomiting and diarrhea. Still, we mustn't forget those two plasmids, pXO1 and pXO2, it acquired in the rainforests of Ivory Coast. It's become a killer, very possibly even for humans.

[1] Leendertz et al: Anthrax kills wild chimpanzees in a tropical rainforest in Nature – 2004
[2] Leendertz et al: A New Bacillus anthracis Found in Wild Chimpanzees and a Gorilla from West and Central Africa in PloS Pathogens – 2006
[3] Hoffmann et al: Persistent anthrax as a major driver of wildlife mortality in a tropical rainforest in Nature - 2017
[4] Köhler: Bacillus anthracis genetics and virulence gene regulation in Current Topics in Microbiology and Immunology - 2002

Hepatitis C Virus in Sharks

There lurks a species of sharks in the dark waters of the western Pacific Ocean: the graceful catshark (Proscyllium habereri). Little is known about this animal. It is an uncommon bottom-dwelling shark found on the shelves of continental and insular waters. The graceful catshark dwells on the sublittoral zone at depths of 50 to 300 meters. Even its food habits are vague to science; it probably feed on bony fishes, crustaceans and cephalopods.
[Foto: Rusty catshark. No image available for the Graceful catshark]

When Chinese scientists investigated an expanded group of potential arthropod and vertebrate host species, that have generally been ignored by other surveillance programs, they found a number of previously unknown viruses[1].

One of these viruses had many similarities with Hepatitis C Viruses. Its polypeptide aligned well with viruses in the genus Hepacivirus (27.9 to 29.3% overall identity).

The scientists named this novel hepacivirus the Wenling Shark Virus. It is named after the Chinese city of Wenling (traditional Chinese: 溫嶺市), a coastal community that has access to the East China Sea. It's also home of their university.

[1] Mang Shi et al: Divergent Viruses Discovered in Arthropods and Vertebrates Revise the Evolutionary History of the Flaviviridae and Related Viruses in Journal of Virology - 201. See here.

Hepatitis C Virus and Type 2 Diabetes

Hepatitis C Virus infection is a widespread condition that affects up to 170 million people worldwide. Liver cirrhosis and hepatocellular carcinoma are well-known complications of Hepatitis C Virus infection, but problems outside the liver develop in up to two-thirds of patients with Hepatitis C Virus[1].
The risk of type 2 diabetes (T2D) and insulin resistance appears to be increased in patients with Hepatitis C Virus as well. The elevated risk for T2D is present both in patients without liver dysfunction and in patients with chronic Hepatitis C Virus-related liver disease[2].

Up to 30% of patients with Hepatitis C Virus have insulin resistance or T2D and patients with Hepatitis C Virus are 1.5 to 3.8 times as likely to have T2D than the general population. Patients with Hepatitis C Virus who are at high risk for T2D due to non-Hepatitis C Virus-related risk factors have an 11-fold greater risk of developing T2D than individuals without Hepatitis C Virus[3]. Epidemiological data largely support the association between Hepatitis C Virus infection and T2D.

Several hypotheses have been proposed to explain how Hepatitis C Virus infection might increase the risk for T2D. According to Dr Tomer, co-author of the study, one way Hepatitis C Virus might influence the development of T2D is through promoting inflammation. “We know that inflammation is associated with T2D, and one hypothesis is that the virus causes inflammation by inducing cytokines, which are inflammatory mediators.”

Another hypothesis is that viral replication within infected cells may disturb normal insulin signaling, particularly in the liver, Dr Tomer said. He added that Hepatitis C Virus may also induce reactive oxygen species and create oxidative stress in the liver, disrupting glucose metabolism and glucose homeostasis.

Lastly, Hepatitis C Virus may not only infect liver cells, but also the pancreatic islet beta cells that secrete insulin, according to Dr Tomer. “Some studies have shown virus-like particles inside the islets,” he said. “But just seeing virus particles does not prove that Hepatitis C Virus infects islet cells. Hepatitis C Virus could be attaching to the cells and not actually infecting them. But this is a very intriguing hypothesis if indeed the virus can somehow cause direct infection of the pancreatic islets.”

[1] Desbois, Cacoub: Diabetes mellitus, insulin resistance and hepatitis C virus infection: A contemporary review in World Journal of Gastroenterology - 2017
[2] Hammerstad et al: Diabetes and hepatitis C: a two-way association in Frontiers in Endocrinology - 2015
[3] Gastaldi et al: Current level of evidence on causal association between hepatitis C virus and type 2 diabetes: A review in Journal of Advanced Research – 2017. See here.

Hepatitis A Virus in Seals

Not so very long ago, scientists believed that primates – including humans - were the only species that were at risk for an infection with the Hepatitis A Virus. Over the last few years, it became evident that other species could also become infected with Hepatitis A Virus or a Hepatitis A-like virus.

At least 13 additional species of the genus Hepatovirus have now been identified[1]. These species infect several small mammals.
Recently, a new Hepatitis A Virus has been discovered in North American harbour seals (Phoca vitulina)[2]. The virus is related to human hepatitis A virus. The researchers tentatively named the virus phopivirus, although my suggestion would be Seal Hepatitis A Virus.

The data support a common ancestry between Seal Hepatitis A Virus and Human Hepatitis A Virus.

[1] Drexler et al: Evolutionary origins of hepatitis A virus in small mammals in PNAS – 2015
[2] Anthony et al: Discovery of a Novel Hepatovirus (Phopivirus of Seals) Related to Human Hepatitis A Virus in mBio - 2015

Hepatitis E Virus in Goats

Hepatitis E Virus in humans is a major cause of acute hepatitis worldwide, primarily transmitted by fecal-oral route. But there are other routes that pose an intrinsic risk to humans.

Zoonotic transmission of Hepatitis E Virus from Hepatitis E Virus infected pigs (uncooked or undercooked pork)[1] or cows (milk)[2] to humans or non-human primates has previously been confirmed. Yes, the Hepatitis E Virus is excreted into milk that is produced by infected cows. Drink it unpasteurised and you're likely to get infected.
The risk of Hepatitis E Virus in goats is only rarely studied. In large parts of China raw mutton and goat milk are traditionally consumed, which means there is certainly a risk of transmission of Hepatitis E virus from goats to humans. The risk of Hepatitis E Virus in goats is only rarely studied.

Now, researchers have studied stool, blood, tissues and milk of goats for Hepatitis E Virus infection investigation in Yunnan Province in China. Not surprisingly, a high prevalence of Hepatitis E Virus infection in goats was found[3]. Analysis revealed that all Hepatitis E Virus isolates from those goats belong to genotype 4 and subtype 4h, and shared a high similarity (>99.6%) with Hepatitis E Virus isolated from humans, swine and cows in the same area.

Which means that Hepatitis E Virus is circulating in at least four different species and that poses a near certainty that the virus will mutate in the foreseeable future.

[1] Meng et al: Prevalence of antibodies to the HEV in pigs from countries where HEV is common or rare in the human population in Journal of Medical Virology – 1999
[2] Huang et al: Excretion of infectious hepatitis E virus into milk in cows imposes high risks of zoonosis in Hepatology – 2016
[3] Long et al: High prevalence of Hepatitis E virus infection in goats in Journal of Medical Virology – 2017

Hepatitis A Virus outbreaks mostly affecting men who have sex with men

Between June 2016 and mid-May 2017, an unusual increase in cases of Hepatitis A affecting mainly men who have sex with men (MSM) has been reported by low endemicity countries in the European Region, and in the Americas (Chile and the United States of America), according to a report by the World Health Organisation (WHO).
In the European Region, 15 countries (Austria, Belgium, Denmark, Finland, France, Germany, Ireland, Italy, the Netherlands, Norway, Portugal, Slovenia, Spain, Sweden, and the United Kingdom) reported 1173 cases related to the three distinct multi-country Hepatitis A outbreaks as of 16 May 2017.

In Chile, 706 Hepatitis A cases were reported at national level as of 5 May 2017. In the United States, the New York City Health Department has noted an increase in Hepatitis A cases among MSM who did not report international travel.

In low endemicity settings, WHO recommends Hepatitis A vaccination for high-risk groups, such as travellers to endemic areas, MSM, people who inject drugs, and chronic liver disease patients. For MSM the main risk factor is related to sexual transmission, particularly oral-anal sexual contact. Most of the affected countries have routinely recommended Hepatitis A vaccine for MSM.

This event is of particular concern from a public health perspective because of the current limited availability of Hepatitis A vaccine worldwide. In addition, several national and international lesbian, gay, bisexual, and transgender (LGBT) pride festivals will take place between June and September 2017, including the World Pride Festival in Madrid, Spain between 23 June and 2 July 2017.

So far, no fatalities have been reported in connection with the ongoing outbreaks. It has the potential to spread further to the general population if control measures (vaccination, hygiene, food safety, and safer sex measures) are not adequately implemented.

Phosphate Fertilizer Kidney Disease

An unknown medical condition has been killing agricultural workers in northern Sri Lanka. The illness is officially described as a 'Chronic Kidney Disease of non-Traditional causes (CKDnT)'.

Patients with CKDnT do not have the commonly known risk factors for kidney disease, such as diabetes and hypertension. Which means that another etiology must be at work here. While northern Sri Lanka is 'blessed' with a hot climate, agricultural workers are not alike the sugar cane workers in Mesoamerica. Chronic dehydration does result in kidney problems and eventually to renal failure.
During the last 2600 years, farmers inhabiting dry zone of Sri Lanka were cultivating rice using irrigated water and organic fertilizer (for our English readers: fertiliser). Now, new varieties of rice cultivated by farmers require large amounts of chemical fertilizers.

Organic or natural fertilizers, such as manure, compost or paddy husk, all contained very low amounts of arsenic. Despite the fact that the import of arsenic containing pesticides is illegal, all tested pesticide brands contained arsenic[1]. There is evidence of a positive association between arsenic exposure and kidney disease mortality[2]. This special type of chronic kidney disease is a toxic nephropathy and arsenic may play a causative role along with a number of other heavy metals. Findings suggest that agrochemicals, especially phosphate fertilizers, are a major source of inorganic arsenic in CKDnT endemic areas in Sri Lanka.
Another possible culprit may be glyphosate (better known as RoundUp), the most widely used herbicide in the disease endemic area and its unique metal chelating properties. While the substance in itself is not considered very toxic to humans, it seems to have acquired the ability to destroy the renal tissues of thousands of farmers when it forms complexes with hard water or nephrotoxic metals[3]. It might even explain similar kidney disease epidemics observed in Andra Pradesh (India) and Central America.

Much more information about Chronic Kidney Diseases of non-Traditional (CKDnT) causes can be found here

[1] Jayasumana et al: Phosphate fertilizer is a main source of arsenic in areas affected with chronic kidney disease of unknown etiology in Sri Lanka in SpringerPlus - 2015
[2] Zheng et al: Arsenic and Chronic Kidney Disease: A Systematic Review in Current Environmental Health Reports – 2014
[3] Jayasumana et al: Glyphosate, Hard Water and Nephrotoxic Metals: Are They the Culprits Behind the Epidemic of Chronic Kidney Disease of Unknown Etiology in Sri Lanka? in International Journal of Environmental Research and Public Health – 2014

High Altitude Kidney Disease

The kidneys are a pair of bean-shaped organs. Each kidney is about the size of a fist. The kidneys' function are to filter the blood in order to remove waste, control the body's fluid balance and regulate the balance of electrolytes.

Loss of kidney function may be acute or chronic. The former is usually reversible, while the latter is permanent.
In high-altitude climbers, the kidneys play a crucial role in acclimatization and in mountain sickness syndromes through their roles in regulating body fluids, electrolyte and acid–base homeostasis[1]. The higher you climb, the lower the amount of oxygen available to your body. The kidneys react to that by temporarily decreasing plasma volume.

There is concern that living at high altitude may accelerate the progression of chronic kidney disease. Many areas of the kidney are marginally oxygenated even at sea levels. Researchers postulated that arterial hypoxemia (abnormally low level of oxygen in the blood) at high altitude poses a risk of faster disease progression in those with preexisting kidney disease[2].

A survey in Tibet to identify the prevalence and associated risk factors of chronic kidney disease in subjects living at altitudes above 3500 meters clearly showed a higher number of people that suffered from High Altitude Kidney Disease[3]. Which suggests that a chronic lack of oxygen causes chronic kidney diseases.

Much more information about Chronic Kidney Diseases of non-Traditional (CKDnT) causes can be found here

[1] Goldfarb-Rumyantzev, Alper: Short-term responses of the kidney to high altitude in mountain climbers in Nephrology, Dialysis, Transplantation – 2014
[2] Luks et al: Chronic kidney disease at high altitude in Journal of the American Society of Nephrology – 2008
[3] Chen et al: Prevalence and risk factors of chronic kidney disease: a population study in the Tibetan population in Nephrology, Dialysis, Transplantation – 2011

Sugar Cane Worker Kidney Disease

An unknown medical condition has been killing male agricultural workers in central America. The illness is officially described as a 'Chronic Kidney Disease of non-Traditional causes (CKDnT)' and it is responsible for 75% of deaths of young and middle-aged men in Nicaragua and El Salvador. Workers in the sugarcane industry are worst affected and the disease has been destroying families and communities since it emerged in the late 1990s. Some researchers suspect that a virus might be to blame as the fields are heavily infested with rodents[1].
Patients experience fever, nausea and vomiting, joint pain, muscle pain, headache, neck and back pain, weakness, and itchiness at the onset of acute kidney disease.

However, further research has now indicated that the epidemic of kidney disease among young Central American males may be the result of continued heat stress and volume depletion[2].

In Nicaragua and El Salvador, age-adjusted mortality rates from kidney disease are among the highest in the world. According to researchers, in these countries, the prevalence of kidney disease (defined as eGFR <60 mL/min/1.73m2).
“Most researchers believe the causes are multifactorial, and it is at least in part related to occupation, given the severe toll that kidney disease is taking on heavy manual laborers in the region,” explained Rebecca Laws, lead author on the study.

For the study, researchers followed 284 sugarcane workers in seven different jobs from one company in Nicaragua. Blood and urine samples were collected before and near the end of the six-month harvest season. Those workers who had the most labor-intensive jobs, cane cutters, had increased urinary NGAL (Neutrophil Gelatinase Associated Lipocalin) and IL-18 (Interleukin-18), both biomarkers of kidney injury.

Researchers observed a protective effect of consuming an electrolyte solution among cane cutters and seed cutters. This indicates there are ways to prevent kidney injury among laborers in high-heat settings.

Global warming might further give rise to the number of cases. Climate change has led to a significant rise of 0.8°C–0.9°C in global mean temperature over the last century and has been linked with significant increases in the frequency and severity of heat waves (extreme heat events)[3].

Much more information about Chronic Kidney Diseases of non-Traditional (CKDnT) causes can be found here.

[1] Murray et al: Mesoamerican nephropathy: a neglected tropical disease with an infectious etiology? in Microbes and Infection - 2015
[2] Laws et al: Biomarkers of Kidney Injury Among Nicaraguan Sugarcane Workers in American Journal of Kidney Diseases - 2015

[3] Glaser et al: Climate Change and the Emergent Epidemic of CKD from Heat Stress in Rural Communities: The Case for Heat Stress Nephropathy in Clinical Journal of the American Society of Nephrology - 2016

Hepatitis E Virus in Niger

On 12 April 2017, the Niger Ministry of Health notified WHO of a Hepatitis E Virus outbreak in the Diffa region, located in the eastern part of the country. On 19 April 2017, the outbreak was officially declared by the Minister of Health.

Since 9 January 2017, an increase in cases of jaundice was noted at the Centre Mere-Enfant de Diffa ('Mother and Child Center of Diffa') among pregnant women. Initially, the cases presented with headache, vomiting, fever, conjunctivitis, pelvic pain and memory loss.

Yellow fever was initially suspected as the cause of this outbreak. However, considering a number of cases among pregnant women reporting to the Mother and Child Center in Diffa and the Hepatitis E Virus outbreak in neighbouring Chad, Hepatitis E Virus was also considered as a potential cause of signs and symptoms. Samples were collected and sent to Institut Pasteur de Dakar (IPD) for laboratory testing. Of the 29 samples tested so far, all tested negative for yellow fever and 15 tested positive for Hepatitis E by PCR.

As of 3 May 2017, a total of 282 suspected cases including 27 deaths have been reported. All reported deaths except for one death are among pregnant women (Case Fatality Rate: 9.6%). To date, five of the six districts in the Diffa region have reported cases, and 188 cases are from the Diffa and N’Guigmi districts. The Diffa region is a region affected by the Lake Chad basin crisis and there is frequent movement across the border.

Hepatitis E Virus in Camels

Hepatitis E Virus is a major cause of viral hepatitis globally. These days zoonotic Hepatitis E Virus is an important cause of chronic hepatitis in immunocompromised patients, but the danger always exists that the virus might mutate enough to target healthy people.
The rapid identification of novel Hepatitis E Virus variants and accumulating sequence information has prompted significant changes in taxonomy of the family Hepeviridae. This family now includes two genera: Orthohepevirus, which infects all mammalian and avian vertebrates, and Piscihepevirus, which infects only one species of fish, cutthroat trouts.

Within Orthohepevirus, there are four species, A-D, with widely differing host range[1]. Orthohepevirus A contains the Hepatitis E Virus variants infecting humans and its significance continues to expand with new clinical information. We now recognize eight genotypes within Orthohepevirus A: HEV1 and HEV2, restricted to humans; HEV3, which circulates among humans, swine, rabbits, deer and mongooses; HEV4, which circulates between humans and swine; HEV5 and HEV6, which are found in wild boars; and HEV7 and HEV8, which were recently identified in dromedary[2] and Bactrian camels[3], respectively. HEV7 is an example of a novel genotype that was found to have significance to human health shortly after discovery.
So, what we now have are two new genotypes: HEV7 or Dromedary camel Hepatitis E Virus (shortened to DcHEV) and HEV8 or Bactrian camel Hepatitis E Virus (shortened to BcHEV). The later is capable of infecting humans (HHEV8) and that means there's another virus that has escaped our detection for quite some time. If it evolves even further, who knows what sort of damage it might do to humans.

[1] Sridhar et al: Hepatitis E Virus Genotypes and Evolution: Emergence of Camel Hepatitis E Variants in International Journal of Molecular Science – 2017
[2] Woo et al: New hepatitis E virus genotype in camels, the Middle East in Emerging Infectious Diseases – 2014
[3] Woo et al: New hepatitis E virus genotype in Bactrian camels, Xinjiang, China, 2013 in Emerging Infectious Diseases – 2017

Hepatitis E Virus in Rabbits

Hepatitis E Virus in humans is a major cause of acute hepatitis in many developing countries in Asia and Africa, where it is transmitted by the fecal–oral route because of poor sanitation practices. Acute hepatitis E is also increasingly reported in industrialized countries, where the transmission is mainly zoonotic.

The initial discovery of Hepatitis E Virus transmission from domestic pigs has been followed by evidence that other mammals, such as wild boars and deer, are also potential reservoirs of Hepatitis E Virus[1][2].
Currently, there are four major genotypes Hepatitis E Virus known that infect mammals from a variety of species. Hepatitis E Virus-1 and Hepatitis E Virus-2 are restricted to humans and transmitted through contaminated water in developing countries. Hepatitis E Virus-3 and Hepatitis E Virus-4 infect humans, pigs and other mammals. The latter two are responsible for sporadic cases of Hepatitis E in developing and industrialized countries. Hepatitis E Virus-3 is distributed worldwide, whereas Hepatitis E Virus-4 largely is found in Asia. Hepatitis E Virus-3 and Hepatitis E Virus-4 infections have been linked to the consumption of raw or undercooked meats, such as pig liver sausages or game meats.

Recent studies have characterized new Hepatitis E Virus genotypes in isolates from rats in Germany, wild boars in Japan, and farmed rabbits in China[3][4][5].

The potential risk for zoonotic transmission of Hepatitis E Virus from rabbits in France is unknown. Cases of autochthonous hepatitis E are commonly reported in France, scientists investigated the prevalence of Hepatitis E Virus in farmed and wild rabbits[6].
One result of the study was that in France farmed and wild rabbits can be infected with Hepatitis E Virus. Analysis indicated that these French rabbit Hepatitis E Virus strain is a new genotype. The identification of a human Hepatitis E Virus strain that is closely related to rabbit Hepatitis E Virus strains reinforced the potential zoonotic risk for infection with this virus.

[1] Meng et al: A novel virus in swine is closely related to the human hepatitis E virus in Proceedings of the National Academy of Sciences – 1997
[2] Meng: Hepatitis E virus: animal reservoirs and zoonotic risk in Veterinary Microbiology – 2010
[3] Johne et al: Novel hepatitis E virus genotype in Norway rats, Germany in Emerging Infectious Diseases – 2010
[4] Takahashi et al: Analysis of the full-length genome of a hepatitis E virus isolate obtained from a wild boar in Japan that is classifiable into a novel genotype in Journal of General Virology - 2011
[5] Geng et al: The serological prevalence and genetic diversity of hepatitis E virus in farmed rabbits in China in Infection, Genetics and Evolution – 2011
[6] Izopet et al: Hepatitis E Virus Strains in Rabbits and Evidence of a Closely Related Strain in Humans, France in Emerging Infectious Diseases - 2012

Hepatitis C Virus mutations 'outrun' immune systems

Unlike its viral cousins Hepatitis A and B, Hepatitis C Virus has eluded the development of a vaccine and infected more than 170 million people worldwide. Approximately 700,000 people die each year from the infection. The creation of a vaccine seems far more difficult that those of its brethren, Hepatitis A Virus and B Virus. Research has now identified a biological mechanism that appears to play a big role in helping Hepatitis C Virus evade both the natural immune system and vaccines[1].
The study found that some mutations occur outside of the viral sites that are typically targeted by antibody responses. Those mutations could also account for the difficulty of making an effective vaccine.

The research discovered that the effectiveness of the antibodies varied, with some viral strains very inhibited by the antibodies and others hardly affected at all. To find out what was causing the variation, the researchers next tapped into the genomes of the Hepatitis C Virus, but found nothing.

The researchers then expanded their search to the proteins on the surface of Hepatitis C Virus. They found that, while mutations in the binding site were not associated with resistance, other mutations in the surface proteins away from the binding site correlated with viruses that persisted despite antibody treatment.

These are the mutations the researchers believe may allow the viruses to avoid being blocked by antibodies altogether. If you think of it like a race, the antibody is trying to bind to the virus before it can enter the cell. These mutations may allow the virus to get into the cell before it even encounters the immune system.

[1] El-Diwany et al: Extra-epitopic hepatitis C virus polymorphisms confer resistance to broadly neutralizing antibodies by modulating binding to scavenger receptor B1 in PloS Pathogens – 2017

Hepatitis A Virus in Himalayan Marmots

Hepatitis A virus (HAV) is a hepatotropic ('liverloving') picornavirus that causes acute liver disease worldwide.

Scientists recently reported the identification of a novel Hepatitis A Virus in Himalayan marmots (Marmota Himalayana) in south-western China. They tentatively named the virus Marmota Himalayana Hepatitis A Virus (MHHAV)[1].
The genomic and molecular characterization of Marmota Himalayana Hepatitis A Virus indicates that it is most closely related genetically to (Primate) Hepatitis A Virus. The virus is morphologically and structurally similar to (Primate) Hepatitis A Virus.

Phylogenetic analysis further indicated that Marmota Himalayana Hepatitis A Virus groups with known Hepatitis A viruses, but forms an independent branch and represents a new species in the genus Hepatovirus.

Evolutionary analysis of Marmota Himalayana Hepatitis A Virus and primate Hepatitis A viruses led to a most recent common ancestor estimate of 1,000 years ago, while the common ancestor of all Hepatitis A-related viruses including phopivirus can be traced back to some 1800 years ago.

The discovery of Marmota Himalayana Hepatitis A Virus may provide new insights into the origin and evolution of Hepatitis A viruses.

[1] Yu et al: A novel hepatovirus identified in wild woodchuck Marmota himalayana in Scientific Reports – 2016

Hepatitis and Energy Drinks

Well, that did take a bit longer than expected. Energy drinks can cause heart problems[1] and even death[2]. That much was already known. But now it appears that the consumption of four to five energy drinks daily for three weeks can already cause painful and potentially fatal hepatitis[3].
A previously healthy man went to his doctor complaining of malaise, anorexia, abdominal pain, nausea, vomiting, generalised jaundice, scleral icterus and dark urine. He was not on any prescription or over-the-counter medications, but reported drinking 4–5 energy drinks daily for 3 weeks prior to presentation.

Laboratory studies showed transaminitis (elevation of certain enzymes in the liver) and evidence of chronic Hepatitis C infection. A liver biopsy showed severe acute hepatitis with bridging necrosis and marked cholestasis (reduction or even stoppage of bile flow).

The development of acute hepatitis in this patient was likely secondary to excessive energy drink consumption. Energy drinks should be considered when patients arrive with acute hepatitis.

[1] Tofield: Energy drinks can cause heart problems in European Heart Journal – 2015
[2] Kaşıkçıoğlu E: Sports, energy drinks, and sudden cardiac death: stimulant cardiac syndrome in Anatolian Journal of Cardiology -2017
[3] Harb et al: Rare cause of acute hepatitis: a common energy drink in British Medical Journal – 201. See here.

Cancer as an infectious disease

If we think about infectious diseases (as opposed to non-communicable diseases) we probably know that these can be caused by viruses, bacteria, fungi, parasites and prions.

Cancer is not on this list. While some viruses can cause cancers in infected hosts, these cancers do not infect others. The cancer dies with the patient or the cure.

But times are changing. Transmissible cancers have been identified as spreading within two vertebrates, dogs (Canis lupus familiaris) and Tasmanian devils (Sarcophilus harrisii), and multiple independent lineages of transmissible cancer have been found in four species of bivalves[1].
[1] Canine Transmissible Venereal Tumor
The first transmissible cancer to be identified was Canine Transmissible Venereal Tumor (CTVT), a solid tumor that spreads within populations of dogs through sexual contact. The etiology of the disease was initially uncertain, but it is now known that transmission occurs through transfer and replication of the cancer cells themselves, rather than through viral modification of cells in each new host. An unexpected feature of CTVT is that it has repeatedly acquired new mitochondrial genomes from its hosts throughout its evolution. Analysis of the CTVT genome found that the cells have been spreading as a transmissible cancer lineage for 10,000–12,000 years[2]. Thus, these cells have been evolving and spreading as an asexual parasitic organism that has outlived its original canine host by more than 500 generations.

[2] Tasmanian Devil Facial Tumor Disease
The first case of Devil Facial Tumor Disease (DFTD) in a Tasmanian devil was found in 1996. DFTD is a solid facial tumor that spreads from animal to animal through physical contact when devils bite each other. It was identified as a transmissible cancer after sequencing of the genomes of DFTD[3]. The fatal disease continues to spread through the devil population and threatens them with extinction.
A recent report identified, a second, apparently completely independent, lineage of DFTD (termed DFT2) in a small number of devils[4]. The original Devil Facial Tumor Disease is now termed DFT1.
[Healthy Tasmanian Devil pup]

[3] Bivalve Transmissible Neoplasias
The finding of transmissible cancer in soft-shell clams and some evidence from disseminated neoplasia in mussels suggested that it could also be transmissible[5]. Recently, disseminated neoplasia was found in mussels (Mytilus trossulus), cockles (Cerastoderma edule) and golden carpet-shell clams (Polititapes aureus)[6].
As multiple lineages of transmissible cancers are spreading through multiple bivalve species, scientists decided to term these diseases 'bivalve transmissible neoplasias' (BTN).

[1] Metzger, Goff: A Sixth Modality of Infectious Disease: Contagious Cancer from Devils to Clams and Beyond in PloS Pathogens – 2016
[2] Murchison et al: Transmissible dog cancer genome reveals the origin and history of an ancient cell lineage in Science – 2014
[3] Murchison et al: Genome sequencing and analysis of the Tasmanian devil and its transmissible cancer in Cell – 2012
[4] Pye et al: A second transmissible cancer in Tasmanian devils in Proceedings of the National Academy of Sciences – 2016
[5] Carballal et al: Neoplastic diseases of marine bivalves in Journal of Invertebrate Pathololy – 2015
[6] Metzger et al: Widespread transmission of independent cancer lineages within multiple bivalve species in Nature - 2016

Hepatitis E Virus in Chad

From 1 September 2016 until 13 January 2017, a total of 693 cases including 11 deaths of acute jaundice syndrome (AJS) have been reported from Am Timan, Chad, a country in the north of Africa, situated south of Libya and east of Sudan[1].
Of the 50 patients with AJS who were hospitalized, 48 were tested for Hepatitis E using the Hepatitis E Virus Rapid Diagnostic Test (HEV RDT) and 27 (56.3%) tested positive. In total, at the end of epidemiological week 2, 2017, a total of 126 tests have been performed, of them 57 (45.2%) were positive, while 69 (54.8%) tested negative for Hepatitis E. 18 (31.6%) of the 57 patients that tested positive using the HEV RDT also had a positive malaria test, and 20 (29%) out of 69 patients that tested negative using the HEV RDT also had a positive malaria test.

Since September 2016, 11 deaths have been reported among the hospitalized cases but the total case fatality might be underestimated.

As of 13 January 2017, 16 pregnant women presenting with AJS have been hospitalized and tested for Hepatitis E, 12 (75%) of them tested positive using the HEV RDT. Of the pregnant women presenting with AJS, four have reportedly died (three had tested positive for Hepatitis E).

Approximately 90% of the AJS cases were reported from Am Timan which appears to be the epi-centre of the ongoing outbreak, and most of the cases are identified through active case findings. As of 13 January 2017, AJS cases have been reported from 59 different quartiers in and surrounding Am Timan.

[1] WHO: Disease outbreak news: Hepatitis E - Chad - January 24, 2017

Hepatitis E Virus and Guillain-Barré Syndrome

Guillain-Barré Syndrome has been abundantly in the news as a potential side-effect of an infection with the dreaded Zika virus[1], but a recent infection with the Hepatitis E Virus may be a cause of Guillain-Barré syndrome (GBS), especially in patients with elevated liver enzymes, researchers reported[2].
Of 73 patients diagnosed with GBS, retrospective study in Belgium, six (8%) tested positive on IgM assays for Hepatitis E Virus. Given the possibility of cross-reactivity with other GBS candidates like cytomegalovirus or Epstein-Barr virus, however, the researchers concluded that 4 patients in the cohort (6%) had GBS likely due to Hepatitis E Virus infection.

Along with related studies from the Netherlands and Japan, this latest study suggest that acute Hepatitis E Virus infection is associated with approximately 5% to 8% of cases of Guillain-Barre syndrome.

Classic Guillain-Barré syndrome and acute inflammatory demyelinating polyneuropathy were the most common clinical and electrophysiologic variants[3]. Neither this study nor the reports from the Netherlands and Japan observed any significant features in terms of patient age, sex, severity or duration of illness, electrophysiological findings or response to therapy (typically intravenous immunoglobulin) to differentiate between cases of GBS that were or were not associated with Hepatitis E Virus infection, the researchers said[4].

More study is needed "to better define the role of this epidemiologically important, and in many areas ubiquitous, agent in neurological diseases," the researchers wrote.

Although it is interesting to know which infection could have triggered GBS in a given patient, there are currently no therapeutic implications.

[1] Uncini et al: Zika virus infection and Guillain-Barré syndrome: a review focused on clinical and electrophysiological subtypes in Journal of Neurology, Neurosurgery and Psychiatry – 2016
[2] Stevens et al: Diagnostic Challenges and Clinical Characteristics of Hepatitis E Virus–Associated Guillain-Barré Syndrome in Journal of the American Medical Association – 2016. See here.
[3] Cornblath: Electrophysiology in Guillain-Barré syndrome in Annals of Neurology - 1990 

[4] Van den Berg et al: Guillain-Barré syndrome associated with preceding hepatitis E virus infection in Neurology – 2014

Flavivirus in Soybean Cyst Nematode

Viruses of the family Flaviviridae have been well documented as the cause of major vector-borne and hepatic diseases in humans. The family currently comprises four genera: Flavivirus, Hepacivirus (Hepatitis B Viruses), Pestivirus and a newly proposed genus Pegivirus.

Viruses of the Flaviviridae have a wide host range that includes both vertebrates and invertebrates. Until recently, the only invertebrate hosts for the flaviviruses were mosquitoes and ticks, which contained viruses exclusively found within the genus Flavivirus. The remaining genera in the family—Hepacivirus, Pegivirus and Pestivirus—are exclusively found in mammals and their diversity has greatly expanded with recent virus discoveries in various mammalian species including bats, dogs, horses, pigs, ruminants and rodents.

Yet, nature always has some surprises in store.
Recently, a flavi-like virus, Soybean Cyst Nematode Virus 5 (SbCNV-5), was discovered from the soybean cyst nematode (Heterodera glycines)[1]. The soybean cyst nematode is a subterranean root pathogen that causes the most damaging disease of soybean in the US.

This novel nematode virus genome was identified in RNA sequencing data from both soybean cyst nematode eggs and second-stage juveniles. Some features of the Soybean Cyst Nematode Virus 5 had homology to pestiviruses in the family Flaviviridae.

The size of the viral genome was exceptionally long (23kb and 19kb, respectively) genomes making it larger than other known pestiviruses. Additionally, the presence of a methyltransferase in the Soybean Cyst Nematode Virus 5 genome is atypical for a pestivirus.

The scientists conclude that Soybean Cyst Nematode Virus 5 is a new flavivirus infecting soybean cyst nematodes.

[1] Bekal et al: A novel flavivirus in the soybean cyst nematode in Journal of General Virology – 2014

Hepatitis C Virus and Tattoos

When you receive a tattoo, your skin is being pierced by a needle and injected with small amounts of ink. Unsterile tattooing can transmit Hepatitis C Virus, and though it is unclear exactly what percentage of people with the virus got it through tattooing, a study found that people with Hepatitis C were almost four times more likely to report having a tattoo, even when other major risk factors were taken into account.
There is not enough research done to determine the exact percentage of people who are diagnosed with Hepatitis C and who got it through tattoos. However, a recent study discovered that people with Hepatitis C were close to four times more likely to report having a tattoo, even when other risk factors were accounted for[1].

If the tattoo was done in a prison or another non-professional setting, the risk was significantly greater[2].

For those responsible enough to go to a professional tattoo parlor where infection control measures are better, there are still health risks to consider. Most people assume that tattoo ink is ‘safe’, but the reality is that the ink is not regulated. The American FDA has received reports of bad reactions to tattoo inks right after tattooing or even years later.

Most colors of standard tattoo ink are derived from heavy metals, including lead, antimony, beryllium, chromium, cobalt nickel and arsenic.

[1] Carney et al: Association of tattooing and hepatitis C virus infection: a multicenter case-control study in Hepatology – 2013
[2] Hellard et al: Tattooing in prisons--not such a pretty picture in American Journal of Infection Control – 2007

Hepatitis viruses are leading killers

Viral hepatitis is one of the leading killers across the globe, with a death toll that matches Aids or tuberculosis, research suggests. A new report estimates that hepatitis infections and their complications led to 1.45m deaths in 2013 - despite the existence of vaccines and treatments[1]. The World Health Organization data shows there were 1.2m Aids-related deaths in 2014, while Tuberculosis led to 1.5m deaths.
Viral hepatitis usually refers to at least five different forms of virus (known as A, B, C, D and E) that can infect humans - some can be spread through contact with infected bodily fluids, while others through contaminated food or water.

Most deaths worldwide (96%) are due to Hepatitis B and C, which can cause serious liver damage (cirrhosis), and predispose people to liver cancer. But, because people don't always feel the symptoms of the initial infection, they can be unaware of the long-term damage until it is too late.

Scientists examined data from 183 countries, collected between 1990 and 2013. They found the the number of deaths linked to viral hepatitis rose by more than 60% over two decades – in part due to a growing population.

Dr Graham Cooke of Imperial College London said: "Although we have vaccines to treat Hepatitis A and B and we have new treatments for Hepatitis C, there is very little money invested in getting these to patients - especially compared to malaria, HIV/AIDS and TB.

The study suggests the problem is biggest in East Asia. But unlike many other diseases, deaths from viral hepatitis were higher in high and middle income countries than in lower income nations.

[1] Stana et al: The global burden of viral hepatitis from 1990 to 2013: findings from the Global Burden of Disease Study 2013 in The Lancet – 2016