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About viruses and viral disease

Events

Virologists take 2008 Nobel in Medicine

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Three virologists have been awarded the 2008 Nobel Prize in Medicine. Harald zur Hausen was recognized for discovering human papilloma virus (HPV), while Luc Montagnier and Francoise Barre-Sinoussi were acknowledged for first isolating human immunodeficiency virus type 1 (HIV-1).

Zur Hausen isolated HPV type 16 in 1983 from women with cervical cancer. A year later he identified type 18; together these two serotypes are found in 70% of biopsies. His work lead to the development of vaccines against the virus. These vaccines have been the topic of some controversy, as we have discussed previously.

Drs. Barre-Sinoussi and Montagnier were part of the group at the Institut Pasteur in Paris that discovered the causative agent of AIDS in 1981. Clearly this was an enormous discovery as the AIDS epidemic has since claimed over 25 million lives. However, what is perhaps as interesting is the omission in this year’s Nobel: Robert Gallo. The latter, working at the NIH, also was believed to have isolated HIV-1, but it is now acknowledged that the Pasteur group was the first to isolate the virus. Apparently the Nobel committee agrees.

Questions on Bioterror Research

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Last week Dr. Bruce E. Ivins, an Army biodefense scientist, committed suicide. He was about to be indicted for murder in connection with the 2001 anthrax-letters incident. His death lead to an article in the New York Times questioning whether the boon in biodefense spending since 2001 has made the country less secure. The logic is that now there are many more laboratories and scientists working in the very dangerous biodefense area. Something is always bound to go wrong, and we may have just multiplied the chances of this happening.

Since 2001 $50 billion has been spent on biodefense laboratories and research. I’ve written before on how this has taken away from basic research on actual, they-are-here-now, pathogens. I’m happy to see these concerns echoed in the Times article and also in a piece in Wired online. 

It’s time to curtail this spending – the most dangerous microbes but the least likely to be seen – and return the money to relevant, investigator-initiated research. The best kind of research there is.

Europic 2008

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Since Monday I have been in Sitges, Spain for Europic 2008. This is a scientific meeting on picornaviruses held every other year in a European country. The picornaviruses are a family of non-enveloped, positive-strand RNA viruses, and includes poliovirus, rhinovirus, and foot-and-mouth disease virus.

I have been attending Europic meetings since 1983, when it was held in Urbino, Italy. Not only is the science excellent and focussed, but the venues are fabulous. Sitges is a lovely town on the coast of the Mediterranean. While the sessions leave little time for seeing the town, it is nice to be in a different place, with old buildings, culture, and a history.

We have already held sessions on virus entry into cells, epidemiology, surveillance, and evolution. I learned yesterday that virus classification is now entirely based on sequence comparisons, with little concern for the biology of the virus. For example, the rhinovirus and enterovirus genera will be combined into one genus called enterovirus. While this change reflects the sequence relationships among the viruses, it will surely be hard to explain why respiratory viruses (rhinoviruses) are classified in a genus whose name implies replication in the enteric tract (enterovirus). The proposed changes in classification can be viewed here.

Another interesting topic was serotyping. Many years ago, new viruses were classified according to an immunological definition: If antiserum against one virus did not neutralize the infectivity of a related virus, they were said to be different serotypes. Modern sequence analyses now indicate that different serotypes are often highly related. Therefore the use of an antigenic classification is somewhat outdated. Sequence analysis will now be used to define serotype, and the different viruses will now be called types, rather than serotypes.

These changes reflect the growing influence of genomics on virology.

Enterovirus 71 Outbreak in Asia

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enterovirus 71There is an ongoing outbreak of enterovirus 71 (EV71) in a broad region of Asia, including China, Vietnam, Mongolia, Taiwan, and Singapore. There have been 3606 cases in China, including 36 deaths.

Infection with EV71 is common in Asia, where it causes hand-foot-and-mouth disease in children, a febrile syndrome accompanied by flat or raised red spots in the tongue, gums, inside of cheeks, palms, soles of feet, and buttocks. Neurological complications of EV71 infection include aseptic meningitis, encephalitis, and poliomyelitis-like polyneuritis. The high fatality rate of the current outbreak is unusual, but not unprecedented. A study of the Taiwan epidemic of 1998 revealed an unusual neurologic manifestation, brainstem encephalitis, which was also observed in Malaysia in 1997 but not in earlier epidemics. The changes in EV71 disease might be a consequence of the emergence of a more virulent viral strain.

EV 71 is a member of the family Picornaviridae, which also contains the well-known pathogen poliovirus. The virus was first isolated in 1969 from a case of fatal human encephalitis in California. EV71 is distributed worldwide and is spread by fecal-oral and possibly by respiratory droplet transmission.

In some locations EV71 is emerging as the most significant neurotropic enterovirus. It has been suggested that the incidence of EV71 might increase after the eradication of poliovirus, in which case there will be increased efforts to develop vaccines and antivirals against this agent.

Chikungunya

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According to ProMED mail, Chikungunya is rapidly spreading in Sri Lanka.

Chikungunya virus is a togavirus in the alphavirus genus. The infection is spread by mosquitos, mainly Aedes aegypti. The viral disease has been known for more than 50 years in the tropics and savannahs of developing countries of Asia and Africa, but never has been a problem of the developed countries in Europe. The disease is uncomfortable (rashes, joint pains), but not fatal. In the last five years, this once third-world viral disease has come into the forefront of public concern.

In 2004, outbreaks of Chikungunya disease spread from Kenya to islands in the Indian Ocean and then to India, where it had not been reported in over 30 years. In 2007, there was an outbreak in Italy, the first ever in Europe. In some of the Indian Ocean islands, more than 40% of the population fell ill.

The reason for the recent spread of Chikungunya disease is that the virus has acquired a new vector, the Asian tiger mosquito Aedes albopictus. A point mutation in the viral genome appears to be the cause for this vector switch. Aedes albopictus is spreading across the globe from eastern Asia and is now found in mainland Europe and the US.

Polio in Nigeria

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Recently there has been an outbreak of polio in Nigeria caused by vaccine-derived poliovirus, VDPV. This outbreak is not unusual except that it is the largest so far caused by VDPV. The first outbreak caused by VDPV was in the Dominican Republic/Haiti in 2001. But the Nigeria outbreak is of interest because it is a continuation of problems begun when the government decided to stop immunization in 2003. Although immunization has since been resumed, coverage has been low. This fact, coupled with the circulation of VDPVs in the region, led to selection of strains of VDPV that could transmit polio among hosts.

The NY Times reported on the Nigeria outbreak on 11 October 2007. Unfortunately the author of the article, Donald McNeil Jr., made two errors in the article. Here is the egregious text:

“But in rare cases it (poliovaccine) can mutate into something resembling wild poliovirus…such mutations are presumably extremely unusual”.

I wrote a letter to the Times Editor to correct these errors, but my words fell upon deaf ears. For the public record, here are my objections:

Dear Editor:

Your article of 11 October, “Polio in Nigeria” contains two errors. The vaccine does not mutate into ‘something resembling wild polio virus’; these mutated viruses are clearly vaccine-derived, not wild poliovirus. Furthermore, such mutations are not ‘extremely unusual’; they occur in nearly every recipient of the live polio vaccine. What is true is that vaccine-associated polio is extremely rare, for which we have no explanation.

Unless the public is provided with correct scientific facts, it cannot be expected to understand the ramifications of outbreaks such as those in Nigeria.