San Diego Hepatitis A Outbreak Infects 481 People

Despite health officials following protocol, one of the largest hepatitis A outbreaks the country has experienced in decades continues to worsen in San Diego. So far, at least 481 people have been infected and 17 have died of the infection in the last year just in this particular outbreak. In Santa Cruz and Los Angeles counties, another 88 cases have been identified. This outbreak is unusual for the USA in that it has been attributed to a lack of basic hygiene and sanitation, with Homeless populations especially impacted, while Hepatitis A is most commonly transmitted through contaminated food. In 2003, 935 people in multiple states were infected with hepatitis A by eating contaminated green onions at a restaurant, and there were no fatalities. It was the largest outbreak since 1998, according to the CDC.

The model for public health officials addressing hepatitis A is to first determine how hepatitis is being spread, vaccinate the at-risk community and make special efforts to improve sanitary and hygienic practices to eliminate fecal contamination. Over the summer, San Diego’s public health officials have shifted focus to sanitation, including hand washing and street cleaning. Streets where nearly 85 percent of confirmed cases were located are being cleaned, pressure washed with bleach in an effort to sanitize any feces, blood, bodily fluids or contaminated surfaces. In September, portable hand-washing stations were delivered in locations where homeless residents tend to congregate. According to Dr. Jeffrey Engel, executive director of the Council of State and Territorial Epidemiologists, these sanitation efforts might not be enough. "I can tell you that washing the door knobs is not going to do it," Engel said. "This is more about human behavior than anything else." This hepatitis A outbreak is complicated by the fact that eliminating a food source will not stop its spread. "You're starting out with a very difficult patient population; probably the most challenging population we have," Engel said. "They don't have any address, they're hard to find and it's a population that's associated with substance abuse and mental illness." I will be looking for future updates to see how effective the sanitation efforts prove to be slowing the spread of hepatitis A.

-       Hannah

Source: San Diego Union-Tribune http://www.sandiegouniontribune.com/news/hepatitis-crisis/sd-me-hepatitis-prevention-20171006-story.html

Viruses vs. Cancer: The WSJ Finds a Way to Weigh In

I'm always really skeptical about reading scientific news in non-scientific publications, but I feel that the experience offers some keen insight to how people consume biology when they presumably haven't learned about it in decades. However, this article puts some emphasis on little known viral facts (at least before I read it). Most notably, it emphasizes that our genome is largely non-coding for protein, yet a rather sizable part of it (8%) is all viral in origin. This normally wouldn't be all that remarkable, but "decoding" the viral genome that has integrated into ours may prove to be useful in inducing a cellular stress response. And that is ultimately what some researchers at Johns Hopkins are trying to do, citing success in reducing tumor size in 20% of patients in a given trial.

This was all amusing to read, but what made me really happy was the final section of the article which specifically mentions that pharma companies are hoping to drug with this approach using epigenetics. One Dr. Baylin says that this therapy is "one possible way" of treating those who don't respond to chemotherapy drugs. The idea is exciting, and I look forward to reading more about the advances they make in anti-cancer, viral therapy. BUT, I'd love to see some of the more technical information, like which viral genes are being expressed? Do immunocompromised cancer patients face a new risk in expressing viral genetic information? Do viruses do more harm than good in this therapy?

Source: https://www.wsj.com/articles/viruses-might-offer-new-help-in-treating-cancer-1455794655

-Andrew  Moreno

2016 Olympics Revisited: It Wasn't Zika?

In the 2016 Olympic Games in Rio, Brazil, there was a lot of discussion regarding the risk of contracting Zika virus for both spectators and athletes alike. The news appeared to be filled with countless stories and fears of contracting Zika virus. However, recent lab results from the University of Utah are suggesting that maybe Zika shouldn't have been getting as much attention in comparison to the viruses that were actually infecting people. Out of the 457 athletes and staff who gave blood samples, only 7% showed signs of becoming infected by any virus carried by mosquitoes. This includes Zika but also other viruses, such as West Nile Virus and Chikungunya. However, none of these tests showed Zika infections. Most of the participants actually appeared to have West Nile Virus, Dengue, or Chikungunya. All of the participants showed mild to no symptoms of these potentially lethal viruses. 

Kro Ampofo, the infectious disease specialist conducting the study at the University of Utah, explains that "Everyone was concentrating on Zika and ignoring that there could be other infections caused by mosquito bites. We did not expect to find so many with these other infections." The researchers and doctors were relieved to have not found any Zika cases. While this is not to say that no one contracted Zika while at the Olympic Games, this study suggests that there are other viruses that are just as, if not more, common that we can't forget about throughout the world. ARUP Laboratories medical director, Dr. Marc Couturier,  explains this issue perfectly: "We all had our Hollywood sunglasses on, and they blinded us to other possibilities. We can't forget that West Nile virus has been around for a while, and is still here." 

Source: https://www.sciencedaily.com/releases/2017/10/171007172948.htm

-Alexandra Ulmer

CCHFV: another tick-spread disease

       Today while hiking Russian Ridge above the Stanford campus,  had to brush through a tight spot between two coyote brush bushes. After getting through I felt a tickling sensation on my arm and looked down to see a tick marching its way up my left arm, looking for a place in my flesh to sink its mandibles and begin sucking my blood. I quickly flicked it off, back into the forest from which it came, and the whole interaction began a discussion within our group about Lyme disease and how many people we knew who had gotten it. 

   In the US ticks are often associated with carrying Lyme disease, but throughout Africa and the middle east as seen below, ticks are associated with  less prevalent but much deadlier disease, Crimean Congo haemorrhagic fever (CCHF). 

   CCHF, which is caused by the Crimean Congo haemoragic fever virus is not pathogenic to the cattle and sheep that the hyalomma genus ticks usually live on, but is very syptomatic in humans, killing about 30% of those that it infects.  Just today in Pakistan, a sixth person died in the country's most recent outbreak of the disease.    

Generally the symptoms of CCHF disease arise suddenly 2-9 days after the initial tick bite. While they begin with a sensitivity to light, muscle pain, headache and dizziness, the disease quickly progresses to include petechial and ecchymoses rashes that bleed into the skin and lead to death within 5 days of illness.

While luckily CCHF has not spread to the Americas, in the last 5 years ticks carrying the disease have been found in farms in Southeast Europe. To save lives and stop the spread of this disease the WHO recommends treating each patient found with CCHF should be treated in the same way as if they had Ebola.

Ref: 

WHO | Crimean-Congo haemorrhagic fever. (n.d.). Retrieved October 8, 2017, from http://www.who.int/mediacentre/factsheets/fs208/en/

Galimand, M., Guiyoule, A., Gerbaud, G., Rasoamanana, B., Chanteau, S., Carniel, E., & Courvalin,    P. (1997). Multidrug Resistance in Yersinia pestis Mediated by a Transferable Plasmid. New      England Journal of Medicine, 337(10), 677–681. https://doi.org/10.1056/NEJM199709043371004

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Your Siblings are Making you Sick!

In the U.S. the CDC estimates that 26,000 children under the age of 5 are hospitalized annually with deaths from influenza ranging from 37 to 171 children each year. This is a particular problem for infants because there is currently no approved influenza vaccine for children under the age of 6 months. They rely on the people around them to be vaccinated (herd immunity).

A recent study from the European Respiratory Journal indicated a link between having more older siblings and infant hospitalization due to influenza. Over 1000 hospitals in Scotland admitting children under 2 were tracked from 2007 to 2015. Researchers found that infants with at least one sibling were 2.5x more likely to be hospitalized, and those with 2 or more siblings were 3 times as likely to be hospitalized. Other factors such as maternal age and maternal smoking were tested, but only being born during flu season had as great a correlation with increased hospitalization due to flu as the number of siblings. This speaks to the ability of larger households to transmit disease to the vulnerable, and underscores the importance of vaccinating the whole family.

https://www.nytimes.com/2017/09/28/well/live/older-siblings-a-risk-factor-for-serious-flu-infections-in-infants.html?rref=collection%2Fsectioncollection%2Fhealth&action=click&contentCollection=health&region=stream&module=stream_unit&version=latest&contentPlacement=13&pgtype=sectionfront

~Scarlett

Our Genes Are Not Our Own!

We've all heard the fun fact that we have more bacterial cells (by pure numbers) than human cells in our bodies. It makes us consider the symbiosis, between ourselves and the natural world, that is salient and essential to human existence. However, no one ever talks about the viruses that have embedded themselves into our genomes and our evolutionary pathways, and played an incredibly important role in the development of the human species as we know it today. Viral DNA makes up approximately 8% of the human genome, with over 100,000 pieces of this foreign DNA lodged into our own DNA. Most of this genetic material comes from retroviruses, which work by inserting their DNA into their host's DNA and then using the cellular machinery to further proliferate. If these retroviruses infect gametes (sperm or egg) their genetic information can potentially be passed on to the next generation, thus cementing them as a new addition to the human genome.

There is still much research to be done on the role of this viral genes in the human context. A virologist at Oxford University named Dr. Katzourakis says "It's not an either or - are these things good or bad? It's a lot more complicated than that." There has been evidence linking this residual retroviral genetic information to development of cancer cells in vitro. However, there are also some viral genes that produce proteins that are essential to reproductive processes. For example, viral genes are responsible for coding proteins called syncytins that play a crucial role in the assembly of the placenta. There is another very important protein called Hemo that is produced by the developing fetus and placenta. It has been hypothesized that Hemo acts as a signal from the developing fetus to the mother, suppressing the mother's immune system so that it does not target the fetus.

Ultimately, we are carrying viruses with us, in our genes and in our evolution. While it still unclear precisely what role they play, we know that there must be some reason this viral DNA has been allowed to persist in our genomes over all these hundreds of thousands of years of natural selection and evolution. This is a growing field of research and it will be exciting to see where it goes within our lifetimes.

-Emma Mathers :)

https://www.nytimes.com/2017/10/04/science/ancient-viruses-dna-genome.html

(A Pop) In(to) Oa(sis)

Currently, AIDS is controlled with drug therapy that targets the actively-replicating virus, however, these drugs aren't able to target the latent HIV hiding in the cell reservoirs. The latent HIV is able to become active and continue to infect the person with the disease, thereby keeping the virus inside them forever. The March 2017 discovery of a protein marker on HIV reservoir cells led to many scientists searching for a way to get ahead of the deadly and clever virus.

Today, researchers from Kumamoto University in Japan have developed a new method to eradicate HIV in viral reservoir cells, named "Lock-in and apoptosis" (Figure 1). 

Figure 1. "L-HIPPO is carried into a cell, with the help of the carrier α-CDE, where it binds strongly to the HIV protein Pr55Gag. This locks HIV virus inside the cell so that it cannot escape via viral budding. The virus is eventually destroyed through apoptosis. Credit: Mikako Fujita"(1)

Using the synthesized compound Heptanoylphosphatidyl L-Inositol Pentakisphophate (or L-Hippo) to bind strongly to the HIV protein PR55Gag, they were able to suppress viral budding. By suppressing viral budding, the researchers were able to trap the HIV virus in the cell and allow for the cell to undergo apoptosis (natural cell death). Associate Professor Mikako Fujita has stated that the approach is not yet available to HIV patients because the research team has to conduct further research on combining the drug therapy that currently exists with this "Lock-in and apoptosis" approach to lead to complete recovery from HIV. Hopefully, this discovery can lead us to an oasis where HIV is finally eradicated!

-Meley Gebresellassie

Sources: 

(1) https://medicalxpress.com/news/2017-10-method-cells-infected-aids-virus.html

(2) https://www.nature.com/articles/s41598-017-09129-w