Tuesday, February 28, 2017

Polio-like virus causing paralysis in over 200 children

Scientists at UCSF, University of Colorado School of Medicine, and the California Department of Public Health have been trying to identify the culprit of a paralyzing virus that has affected more than 200 children since 2014, including many Bay Area children. In humans, the course of the illness began with a flu-like syndrome followed by paralysis in one or more limbs that resulted in permanent damage. In 2014, 120 cases were found in 34 states. Only 21 cases occurred in 2015, which is apparently on par with the national average. However, in 2016, 132 cases of sudden paralysis were reported in 37 states. This points to a cyclical nature in the virus’ life cycle, which we’ve encountered for many viruses in this course.

Scientists suspected that the culprit virus would be an enterovirus since the symptoms resembled poliomyelitis. A few children tested positive for Enterovirus D68, but the association with the disease appeared to be weak. However, Enterovirus D68 has been increasing in prevalence in the United States, which has renewed interest in investigating the virus.

It had been discovered that the virus had been mutating since the 1960s that have resulted in an increase in virulence and possibility of causing paralysis. Lab mice exposed to the new strains Enterovirus D68 developed paralysis in at least one limb a few days later. Exposure to the old strains of Enterovirus D68 did not produce the same result. Autopsy of the exposed mice showed that the virus was located in the cells of the spinal cord that control the paralyzed limbs. This provides a possible explanation for why the virus couldn’t be isolated in most of the children’s spinal fluid. Perhaps if spinal cord biopsies were taken, the virus could have been isolated sooner. However, spinal cord biopsies are extremely risky.

A promising finding from these studies is that mice given antibodies from exposed mice appeared to be protected from the virus, which points to the possibility of developing a vaccine.

~Jazzmin


Read more here: http://www.sfchronicle.com/health/article/Science-closing-in-on-polio-like-virus-that-10961180.php

Sunday, February 26, 2017

Zika Virus Linked to Testicular Atrophy

Following the 2015-2016 Zika outbreak, the virus was found to persist in the semen of infected individuals for months. Until recently, it was unclear how the virus affects the testes. A study published this week suggests that Zika virus infection causes progressive testicular atrophy.

To further understand the effects of Zika infection, the researchers injected mice with Zika virus. Even after clearance from the blood, high levels of viral RNA and antigen were found in the epididymal lumen, where sperm is stored, and in surrounding epithelial cells. 21 days after infection, the testes of Zika-infected mice were significantly smaller than those of control mice. In addition, these mice had reduced levels of serum testosterone, suggesting that male fertility may affected.

-Sally Tran

References:
Kashef Z. "Zika virus harms testes, says study." Yale News. 2017. news.yale.edu/2017/02/22/zika-virus-harms-testes-says-study

Uraki R, Hwang J, Jurado KA, et al. "Zika causes testicular atrophy." Science Advances. 2017 Feb 22; 3(2):e1602899. doi: 10.1126/sciadv.1602889

Soulmates for Rat Lovers: Seoul Virus

News outlets have become concerned with a recent outbreak of Seoul virus connected with rat breeding facilities. So far 16 people have been infected and there have been three reported cases of hantavirus hemorrhagic fever with renal  syndrome (HFRS).  This outbreak is concerning as it is a multi-state outbreak, and while transmission from human-human has not been documented, the rarity of the disease coupled with the severity of complications have CDC officials working to curb the outbreak as fast as possible.

What exactly is Seoul virus?

Seoul virus is a species of virus within the hantavirus genus, which is a part of the viral family Buynaviridae.  Hantaviruses spread by contact with rodents, and includes viruses that are fatal to humans.  However, since there does not exist a vaccine or a treatment for Seoul virus infections, preventing infection is essential.  Of the people infected so far, none have died, and the fatality rate is only estimated at 1-2% of people infected.

Current research around Seoul virus has been looking into the importance of terminally deleted RNAs, which were shown to accumulate in cells infected with Seoul virus.
Image/National Park Service


-Cynthia Taylor

Fields, Bernard N, David M. Knipe, and Peter M. Howley. Fields Virology. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins, 2013. Internet resource.


Saturday, February 25, 2017

Mathematicians Invade Virology

Move over, next-generation sequence advocates. The mathematicians are here, with a grand new way to classify viruses: CAPSID MORPHOLOGY! ...

-- wait, what? --

Yes, that's right. Classification based on capsid structure is back. 

Let's backtrack to make sure you're caught up. Way back when, say, 100 years ago, when viruses could only be studied under the microscope, classification was based on structure. We now know that most viruses have icosahedral and helical capsids, with some having more complex morphology. However, many viruses are also enveloped, so they basically just look like blobs under EM imaging. 

When PCR and sequencing techniques were refined, sequencing took over as the main classification technique. Phylogenetic trees could be constructed, and viral lineages could be traced. 

However, as we understand how DNA influences proteins, i.e. the capsids, mathematicians have stepped in to help connect how capsid shape can be used to understand both DNA and viral ancestry. A new highly-sensitive computational prototype tool has been developed by a team at the University of Helsinki, and can be used to determine amino acid structure from the capsid protein. 

Honestly, I'm not too convinced. If we know all genetic information about a virus, I believe we have more information than just the capsid gene. However, I'll leave it up to the experts to guide the rapidly changing field of virus classification.

News Article:
https://www.sciencedaily.com/releases/2017/02/170223101847.htm 
Research Paper:
http://jvi.asm.org/content/early/2017/01/19/JVI.02275-16

-- Sharon Kam

The Old Adage SolveD: Vitamin D & Colds

A study published recently has confirmed it all: Vitamin D does in fact promotes immunity against colds and the flu!

Vitamin D has long been known in promoting bone and muscle health. However, Dr. Martineau, from the Queen Mary University of London, led a group to investigate further about Vitamin D's functions.  Study participants took daily or weekly doses of vitamin D supplements, and the data shows the daily or weekly supplements can halve the risk of acute respiratory infection -- this includes the common cold and flu viruses!

These findings correlate with previously known Vitamin D effects. For instance, Vitamin D is known to protect against asthma attacks. A possible reason? Vitamin D decreases viral infection causing acute respiratory disease, a common cause of asthma.

Colds and the flu are most common in winter and spring months, when there is least amount of natural Vitamin D (no sun, no Vit D). Take your supplements, kids!

News Article:
https://www.sciencedaily.com/releases/2017/02/170216110002.htm
Research Paper:
http://www.bmj.com/content/356/bmj.i6583

-- Sharon Kam

Viral Link to Multiple Sclerosis?

At the Americas Committee for Treatment and Research in Multiple Sclerosis 2017 Forum this past Friday, a number of scientists presented the idea of viral infections leading to an increased risk for Multiple Sclerosis. Multiple Sclerosis is a debilitating disease where the immune system attacks myelin that functions as protection for our nerve fibers and has a cause that has not been fully established. Recently, however, human endogenous retroviruses (HERVs), HHV-6, and EBV have been highlighted as leading to a higher chance of attaining Multiple Sclerosis.
One study, conducted by Antonina Dolei at the Universita’ degli Studi di Sassari, discussed how HERVs, particularly MSRVenv and Syncytin-1 led to a hyperactivation of the immune system and may work to develop MS. Also, in this study the researchers found that MS patients consistently had HERV-W/MSRV in their blood samples, which then highlights the possibility of using these viruses as biomarkers.
Another study was conducted by Steve Jacobson, who is the Chief of the Viral Immunology Section at the NIH, and he looked at the role that HHV-6 has with MS. While HHV-6 is a very ubiquitous virus, it was also consistently found in MS lesions and outside the brain during MS clinical exacerbations. However, given the ubiquitous nature of the virus, it is hard to establish a strong link between the virus and MS.
Lastly, another study by Alberto Ascherio from Harvard School of Public Health looked at EBV and MS. He found that there was a 10-and 20 fold increase in risk for MS in those individuals that had EBV infection either during childhood or later in life. One again, there isn’t sufficient information to establish a direct link.
In conclusion, more research is being done to see what role viruses might be playing in Multiple Sclerosis development and more will need to be done in order to gain a clearer understanding.

-Jeanette Rios

Wednesday, February 22, 2017

13 person HIV vaccine trial



IrsiCaixa AIDS Researhc Insisiute, with support from Obra Social “la Caixa,” the Department of Health of the Generalitat de Catalunya, and Fight AIDS Foundation have seemed to have found “a functional cure” for HIV. The trial is small (with five successful subjects) and does not have a control group.

The trial has shown that the developed vaccine can boost the immune system enough to allow infected people to regulate the levels of HIV enough to bring the viral load down. The way Mothe, the clinician who presented the results described it is as,”re-[educating] our T cells to control the virus.”

From the 13 people that started in this study, which consisted of of antiretroviral therapy followed by a tripartite shot regimen followed by a cease of the antiretroviral therapy, 5 of them were able to effectively maintain virus levels down from 6-28 weeks. However, in 8 of the 13 original subjects had the virus return after 4 weeks, which is usually the case. Compared to other vaccines, which have previously only managed to maintain 10% of subjects with controlled levels of virus, this 38% rate seems monumental. The main method employed by the vaccine had been through mechanisms to reeducate the host immune system to control the virus, while not on antiretroviral therapy.

The vaccine being developed in this trial claims to be successful due to the “highly conserved” internal structures and enzymes. Before the vaccine, only 4% of host cytotoxic T cells targeted these conserved proteins and enzymes and after the vaccine over 67% of cytotoxic T cells targeted conserved proteins and enzymes.

Gianna Nino-Tapias ('18)

Reference:
- Cohen, J. “AIDS vaccine may be ‘functional cure’ for some. Web. Science (2017). Accessed 22 February 2017. < http://www.sciencemag.org/news/2017/02/aids-vaccine-may-be-functional-cure-some>
- press.lacaixa.es/socialprojects/show_annex.html?id=59909

TORCHES and Autism

A research team at Columbia University and in Norway conducted a cross-control epidemiological study to determine links between known teratogenic infections and autism. The team used data from the Norway Autism Birth Cohort, which was composed of 442 mothers of autistic children and 46 mothers of non-autistic children from 1999 to 2008, matched for sex and month and year of birth. Blood samples were taken from the women taken at midpregnancy and at the time of birth to check for CMV, Toxoplasma gondii, rubella, HSV-1, and HSV-2.

The researchers found that HSV-2 infection at midpregnancy was associated with a 2x increase in risk for autism in male babies. No other associations were found and the study was underpowered to make associations for girls.

This study, while important, doesn’t make any definitive conclusions about risk factors for autism. Some scientists think that an inflammatory response in the fetus due to stress would cause autism. For example, a Swedish study showed that hospitalization during pregnancy was associated with a 30% increased risk of autism for the baby. Other scientists believe infectious vectors must be at play since autism requires drastic restructurings of the neocortex.


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Read more here: http://www.sciencemag.org/news/2017/02/herpes-virus-may-be-trigger-autism

-Jazzmin