National Institutes of Health National Institute of Allergy and Infectious Diseases: EMBARGOED FOR RELEASE Thursday, Jan. 1, 1998 4:00 p.m. Eastern Time
John Bowersox (301) 402-1663 jbowersox@nih.gov

"This is an interesting finding that uncovers yet another strategy that viruses use to protect themselves from harsh environments," says NIAID Director Anthony S. Fauci, M.D.

The molluscum contagiosum virus (MCV) causes a persistent and sometimes disfiguring skin disease common among HIV-infected individuals and others with weakened immune systems. In 1996, researchers led by Bernard Moss, M.D., Ph.D., chief of NIAID's Laboratory of Viral Diseases (LVD), reported the entire genetic sequence of MCV. Analysis of the MCV genome revealed a viral gene whose sequence was very similar to that of the gene for an important human enzyme, glutathione peroxidase. This enzyme neutralizes caustic chemicals called peroxides made by immune system cells to fight infection.

In the Jan. 2, 1998 issue of the journal Science, Dr. Moss and colleagues from the LVD and Harvard Institutes of Medicine in Boston, Mass., report that the MCV gene, like its human counterpart, encodes a protein that contains selenium, a relatively rare element found in only a small number of proteins. Previously, none of these so-called selenoproteins had been identified in viruses.

When the researchers engineered human cells to express the MCV selenoprotein, these cells were largely protected from exposure to UV radiation and peroxides. Ordinarily, explains Dr. Moss, UV radiation and peroxides are cytotoxic, causing cells to die through a process known as apoptosis.

These findings notwithstanding, Dr. Moss and his colleagues note that it is too early to determine definitively the actual role the selenoprotein plays within the virus. The lack of a good animal model of MCV infection and the virus's inability to grow in tissue culture hinder efforts to find this information. However, the researchers speculate that since MCV resides exclusively in human skin, the virus "captured" the selenoprotein gene as a means of defending itself against ultraviolet radiation and the immune system.

Based on the fact that the sequence of the MCV gene is nearly 75 percent identical to the sequence of the human glutathione peroxidase gene, they also speculate that the virus acquired the gene relatively recently in its evolutionary history. Other MCV genes that share sequence similarities with known human genes are only 20 to 25 percent identical to their human counterparts.

"This would seem to be a clever ploy for a virus that replicates in the epidermis," Dr. Moss and his co-authors conclude. Dr. Moss adds that in addition to advancing our understanding of how MCV interacts with its human host, this finding could provide useful insights into the workings of the human glutathione peroxidase enzyme. In future studies, he and his colleagues will continue to characterize and compare the viral and human proteins.

In addition to Dr. Moss, collaborators on this study included Joanna L. Shisler, Ph.D., and Tatiana G. Senkevich, Ph.D., both of the LVD, and Marla G. Berry, Ph.D., of the Harvard Institutes of Medicine in Boston, Mass. Dr. Berry's research was supported by a grant from the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK).

NIAID supports research on AIDS, malaria, tuberculosis and other infectious diseases, as well as allergies and immunology. NIAID and NIDDK are components of the National Institutes of Health (NIH), an agency of the U.S. Department of Health and Human Services.

Reference:

Shisler JL, Senkevich TG, Berry MJ, Moss B. Ultraviolet-induced cell death blocked by a selenoprotein from a human dermotropic poxvirus. Science 1998;279:102-105.

Press releases, fact sheets and other NIAID-related materials are available on the Internet via the NIAID home page at http://www.niaid.nih.gov.

980101
NIH98011

Published 1998 - National Institute of Allergy and Infectious Diseases . All material contained in this report is in the public domain and may be used and reprinted without special permission; citation to source, however, is appreciated.

AEGiS is a 501(c)3, not-for-profit, tax-exempt, educational corporation. AEGiS is made possible through unrestricted funding from Broadway Cares/Equity Fights AIDS, the Elton John AIDS Foundation, National Library of Medicine, and donations from users like you.

Always watch for outdated information. This article first appeared in 1998. This material is designed to support, not replace, the relationship that exists between you and your doctor.

AEGiS presents published material, reprinted with permission and neither endorses nor opposes any material. All information contained on this website, including information relating to health conditions, products, and treatments, is for informational purposes only. It is often presented in summary or aggregate form. It is not meant to be a substitute for the advice provided by your own physician or other medical professionals. Always discuss treatment options with a doctor who specializes in treating HIV.

Copyright ©1980, 1998. AEGiS. All materials appearing on AEGiS are protected by copyright as a collective work or compilation under U.S. copyright and other laws and are the property of AEGiS, or the party credited as the provider of the content. .