TWiV 436: Virology above Cayuga’s waters

At Cornell University in Ithaca, New York, Vincent speaks with Susan, Colin, and Gary about the work of their laboratories on parvoviruses, influenza viruses, and coronaviruses that infect dogs, cats, horses and other mammals.

You can find TWiV #436 at, or listen below.

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TWiV 364: It’s not SARS 2.0

On episode #364 of the science show This Week in Virology, Vincent, Rich, and Kathy speak with Ralph Baric and Vineet Menachery about their research on the potential of SARS-like bat coronaviruses  to infect human cells and cause disease in mice.

You can find TWiV #364 at

TWiV 215: Illuminating rabies and unwrapping a SARI

On episode #215 of the science show This Week in Virology, Vincent, Alan, and Kathy review the finding that rabies virus infection alters but does not kill neurons, and provide an update on the novel coronavirus in the Middle East.

You can find TWiV #215 at

XMRV in human respiratory tract

An important question about the retrovirus XMRV, which has been implicated in prostate cancer and chronic fatigue syndrome, is where the virus replicates in humans. Such information would provide clues about how infection might be transmitted. To date the virus has been detected in malignant prostate cells and in the peripheral blood mononuclear cells and plasma of patients with CFS. A new study reveals that XMRV is present in respiratory secretions.

Polymerase chain reaction was used to detect XMRV in 267 respiratory samples taken from German patients. One group comprised sputum and nasal swab specimens from 75 travelers from Asia who had respiratory tract infections. The second group consisted of 31 bronchoalveolar lavage samples from patients with chronic obstructive pulmonary disease, while samples from the third group were from 161 immunosuppressed patients with severe respiratory tract infections. The study included 62 healthy controls. It should be noted that none of the patients had been diagnosed with CFS.

XMRV sequences were detected in 3 of 75 samples (2.3%) in group 1, 1 of 31 samples (3.2%) in group 2, and 16/161 (9.9%) in group 3. Six of the XMRV-positive samples in the second group also contained rhinovirus, adenovirus, or pathogenic fungi. The higher rate of detection of XMRV and other microbes in immunosuppressed individuals is not unexpected. The control group contained 2 of 62 samples (3.2%) positive for XMRV.

The presence of XMRV in PBMCs and plasma suggests a blood-borne route of transmission of the virus: transfusions, health care associated needle sticks, and intravenous drug use. Does finding XMRV in the respiratory tract prove that the virus can be transmitted by the respiratory route? No, not until we have other information, including the level of virus in respiratory secretions, and the infectivity of XMRV. In this context it is interesting to note that it was not possible to isolate infectious XMRV from the respiratory tract of the German patients.

Reviewing the transmission of another human retrovirus, HIV-1, is instructive in understanding the pathogenesis of XMRV infection. The main modes of transmission of HIV-1 are sexual, parenteral, and from mother to infant. These routes of transmission are consistent with levels of infectious virus in body fluids (shown in this table). Viral RNA can be detected at several levels of the respiratory tract, but respiratory secretions rarely transmit HIV.

FIsher, N., Schulz, C., Stieler, K., Hohn, O., Lange, C., Drosten, C., & Aepfelbacher, M. (2010). Xenotropic murine leukemia virus-related gammaretrovirus in respiratory tract Emerg. Inf. Dis. : 10.3201/eid1606.100066

Poliovirus is IRESistable

Our latest paper has just been published in the Journal of Clinical Investigation. The title of the paper is “Poliovirus tropism and attenuation are determined after internal ribosome entry”. This is the work of a Ph.D. student in my laboratory, Steven Kauder.

If you would like a nice summary of this work, there is an excellent commentary by Bert Semler in the same journal, entitled “Poliovirus proves IRES-istible in vivo“. The title of this commentary is a play on the main theme of the research paper: the Internal Ribosome Entry Site (IRES) of poliovirus. The poliovirus IRES is an RNA sequence at the 5′-end of the viral genome that allows ribosomes to bind internally, rather than threading on the 5′-end as they do for most mRNAs. In our paper, we show that poliovirus attenuation and tropism are not determined by the viral IRES.

Let’s back up a bit to explain this last statement. Viral tropism is defined as the tissues in which a virus replicates. Poliovirus, the causative agent of poliomyelitis, infects very few tissues in humans: the intestine, the brain and spinal cord, and perhaps one other site. A restricted tropism is in fact a common property of many viruses. What restricts viral multiplication to so few tissues has been a long-standing question in virology. For poliovirus, it was first believed that the restricted tropism was a consequence of where the virus receptor is located. The virus receptor is a cell surface protein that is needed to bind the virus particle and bring the genetic material of the virus into the cell. However, some time ago it was shown that the receptor for poliovirus does not determine the narrow tropism of the virus. Subsequently it was suggested that the viral IRES might control the tropism – but in this recent paper we show that this is not the case.

The other topic of our paper concerns the live poliovirus vaccine, also known as the Sabin vaccine or oral poliovirus vaccine (OPV). There are three different vaccine strains of poliovirus, all isolated by Albert Sabin. The genetic material of each vaccine strain contains mutations, or genetic changes, that prevent it from causing disease. When the Sabin vaccines are ingested, they replicate in the intestine and provide immunity to infection, but they do not cause polio. Precisely how these mutations ‘work’ has been a matter of considerable debate. It has been believed that the mutations change the properties of the viral IRES so that it continues to direct translation in the human gut, but not in the spinal cord and brain. In our paper we show that this hypothesis is wrong. A mutation in one of the three Sabin vaccine strains actually weakens the virus in all tissues.

I recognize that much of this description may be beyond the understanding of someone who is not a scientist. A goal of this weblog is to make virology accessible to everyone. Therefore in the coming weeks I will endeavor to provide the background needed to understand this and similar material that will appear here.