Wednesday, May 20, 2015

Norovirus outbreak on ship departing from San Francisco

An outbreak of norovirus occurred last week on a Princess Cruise ship departing from nearby San Francisco en route to Hawaii.  Of the 3,681 people on board, over 150 passengers and crewmembers were infected with the virus aboard the Star Princess.  Norovirus was detected in preliminary tests collected onboard the ship, and  stool samples have been collected and sent to the CDC for further testing.

After detection, sanitation procedures were ramped up to prevent further transmission of the virus. Passengers were also advised of ways to minimize transmission and their risk of infection, including washing their hands thoroughly, and using only restrooms in their cabin.  Furthermore, passengers were not allowed to disembark the ship, due to the possible risk of transmission.  Upon its return to San Francisco, the ship was thoroughly cleansed in preparation for its next cruise.

This latest outbreak has further affirmed the reputation of cruise ships as a breeding ground for extremely contagious pathogens such as Norovirus.  In fact, this incident represents the sixth time in 2015 that a cruise ship has reported a Norovirus outbreak en route to a US port.  The Princess Cruise line is no stranger to Norovirus outbreaks; in 2014 alone, outbreaks operated by Princess Cruises accounted for seven of the sixteen documented outbreaks on cruise ships in 2012.

--Andrew Duong

Wednesday, May 13, 2015

Rabies in Brain Imaging

We spent a bit of time talking about rabies in Humans and Viruses. A scary zoonotic infection that kills if untreated, rabies has been a scourge of humanity since ancient times. Over the past few years however, Ed Callaway of the Salk institute has been working with a deletion mutant strain of rabies with a GFP gene added. Rabies infects neurons through axon terminals and spreads backward (i.e. in a retrograde direction). This mutant strain replicates within host cells, but cannot spread beyond the first neuron they infect. Thus, the vector is not only safe, but it also doesn’t lead to any background fluorescence other than that which comes from the cells it infects.


Monday, May 11, 2015

Rift Valley Fever Virus Helps Understand Viral Replication

A group in Montreal, Canada is attempting to understand hemorrgaic fever viruses through the lens of basic research. By understanding the mechinism by which the viruses replicate adn mutate, they hope to create possible drug targets for future therapeutics which may be a more economically viable solution to such diease than a vaccine (vaccines have been difficult to finance becasue many of these viruses occur in poor countries where there is not a large enough financial incentive for large scale produciton).

Using Rift Valley Fever Virus, researches attempted to characterize the method of replication of the virus. Using nuclear magnetic imaging (NMR), the researches attempting to characterize what each of the viral proteins were responsible for  replication. They discovered that a non-structural protein (NSs) of the virus binds to Transcription Factor II in the cell and creates nuclear filaments. The viral protein that does this looks similar to the human DNA repair proteins (sharing similar structural motifs) and may be a potential candidate for drug-targeting, since inhibiting the protein's action reduces virulence.


Mutagenesis Induction in Viruses

Viruses - particularly retroviruses like HIV - are notorious for their ability to mutate.  The rapid replication of viruses paired with their high mutation rate allow viruses to adapt to their host quickly. However, mutations are only beneficial to a certain extent, and most mutations are likely maladaptive.  Using this information, scientists at the University of Chicago and MIT have been able to induce mutagenesis in viruses, increasing their rate of mutation to a point where the virus can no longer function effectively.  Moreover, these scientists have developed a spectroscopy method that further elucidates the mechanism behind nucleotide analogs.

The researchers used an anti-HIV agent called KP1212 that evades viral detection and infiltrates a viruses genome.  KP1212 functions essentially as a nucleotide analog that mimic DNA bases and result in mismatching of the normal adenosine-thymine, and cytosine-guanine base pairings in DNA. KP1212 is believed to work by repositioning hydrogen atoms in DNA, and resulting in faulty hydrogen bonding.

The use of two-dimensional infrared microscopy by the scientists to examine the structure of mutated viral DNA is novel, as scientists typically use nuclear magnetic resonance.  The benefit of infrared microscopy is that scientists can examine the quickly changing structures of mutagenic viral DNA in aqueous solution (the natural environment of cells) as opposed to organic solvents.  The ability of infrared microscopy to detect different mutagenic viral DNA structures, which quickly change shape and are keenly sensitive to time-changes, has resulted in the discovery of many different tautomers invoked by the KP1212 molecule.


--Andrew Duong

Ebola found in the eye of "cured" patient

Following up on last week's post about the alleged sexual transmission of Ebola through a previously infected man's sperm, a new report this week has found a new potential reservoir for Ebola: the inside of a person's eye.  The eye is a prime place for a virus to reside because the inside of the eye (alongside the testicles) exhibit immune privilege, a phenomenon wherein certain immune molecules and compounds are found at lower concentrations in these areas.  Ebola was found in the eye of Dr. Ian Crozier, an American doctor who was infected with Ebola, and "recovered" from the virus in October.   However, months later, high pressure in his eye developed, resulting in blurred vision and discomfort for Dr. Crozier.  Knowing that Dr. Crozier was once infected with Ebola just a few months ago, opthalmologists at Emory University drew fluid from the inside of his eye to test if Ebola was responsible for the pressure build-up inside his eye.

Surprisingly, laboratory tests revealed the presence of Ebola in the inside of the Dr. Crozier's eyes, but not in his tears or surface film, meaning that while Ebola persisted in his system, his potential to infect others was very low.  With no approved treatments for Ebola, Dr. Crozier's condition deteriorated rapidly.  In a particularly gruesome incident, Dr. Crozier's eye changed color from blue to green for several weeks.  Eye color change is extremely rare for viral infections, and usually indicate a severe infection.  Scientists are preliminarily dubbing the new eye condition post-Ebola syndrome, as reports from West Africa suggest that other recovered patients have experienced similar eye problems.

Luckily for Dr. Crozier, an experimental treatment consisting of steroids and an antiviral has resulted in his gradual recovery, showing promise for treatments currently in development against the virus. His eye color, for example, reverted back to its natural blue color, and parts of his vision are returning.  However, it is still too early to tell what the long-term effects of Ebola are, and if Dr. Crozier will ever fully recover from the disease.  Future research is critically needed to study the chronic effects of Ebola, especially given that there have been relatively few infections and even fewer survivors prior to the 2014 West African Ebola outbreak.


--Andrew Duong

Wednesday, May 6, 2015

Are Dangerous Viruses Just Horsing Around? Neigh...

--Google Images

The recent Kentucky Derby featured superbly athletic horses at the prime of their lives. Unfortunately, not all horses (or other livestock for that matter) are so fortunate. In the past week, 2 stories have been hoofing around the news. The first has been an outbreak of vesicular stomatitis virus, a rhabdovirus like the infamous rabies. It primarily infects insects and livestock, but it can be a zoonotic disease of humans that consists of flu-like symptoms. VSV has also been studied as a candidate for virus-based vaccine therapy (
            In Kane County, Utah, several horses and a mule have become sick with VSV. While many animals recover from vesicular stomatitis, it can cause lesions in the animals’ mouths and on their hooves that cause them pain. It also causes them to show a severe decrease in appetite, which is especially problematic for dairy cows and other animals who are supposed to grow fast and/or be in good physical condition. While the exact means of transmission isn’t known, it is thought that saliva and fluid from ruptured blisters are a likely mechanism. Seeing as rabies is also transmitted via saliva, this seems plausible.

--Vesicular Stomatitis Virus, from Wikimedia Commons

            In Oregon, four horses have tested positive for equine herpes virus (EHV-1). Herpesviridae, as we’ve learned, is a very old and successful group of viruses that infect a myriad of different species. These viruses can cause a wide variety of symptoms (remember the 9 human herpes viruses?).

--EHV-1, from

 Like all herpesviruses, it can go latent and then reactivate to cause clinical disease. Horses infected with EHV-1 can suffer from respiratory and neurologic symptoms (e.g. loss of muscle tone), as well as fever, urine dribbling and nasal discharge. In severe cases, the animal may die, or a pregnant mare may abort her fetus. The symptoms are treatable, but as is the case with human herpes viruses, “unlike love, herpes is 4ever”™. While humans aren’t in any danger from the virus, they can spread it on their clothing and equipment.


Sunday, May 3, 2015

Sexual Transmission as a Possible Route of Infection for Ebola

More evidence of sex as a possible mode of transmission for the Ebola virus recently emerged out of Liberia this week.  A Liberian woman contracted the virus in March despite having no contact with deceased Ebola victims or those displaying Ebola-like symptoms, and no travel history to countries where Ebola is currently active.  However, this woman did have unprotected vaginal intercourse with an Ebola survivor a week before she developed symptoms, leading investigators to suspect sex as the mode of transmission.

Sexual transmission of the virus has long been suspected, as the virus has been found to linger in the sperm of men for up to 101 days after development of symptoms.   However, if sexual transmission is indeed the route of transmission in this case, it may indicate that the virus can persist for much longer in the sperm; the man developed symptoms 199 days - more than 6 months - before having sex with the woman.

It should be noted, however, that another woman who had sex with this man between February and March did not contract the disease.  Furthermore, there was no mention that the virus was actually found in the survivor's sperm.  As a result, it is possible that the virus was not contracted sexually, particularly because the screening process for risk factors relies the investigators asking the right questions, and the respondent recounting his or her experiences accurately.

The CDC currently recommends the use of condoms when having sex and avoidance of coming into contact with the semen of a male survivor to prevent sexual transmission of Ebola.

--Andrew Duong