November 16, 2005
Tips from the journals of the American Society for Microbiology
Researchers have identified a gene in the Epstein-Barr virus that may contribute to the development of lymphoproliferative disease (LPD) in humans. Their findings appear in the November 2005 issue of the Journal of Virology.
Epstein-Barr virus (EBV) is a form of human herpes virus that is the causative agent of mononucleosis. It is often associated with various types of human cancers, specifically lymphoproliferative disease (leukemia and hodgkins/non-hodgkins lymphoma), in immunosupressed patients. In the study immunodeficient mice infected with an EBV mutant missing a gene that controls cell lysis (the rupturing of the infected cell to release new viruses) did not develop LPD, however, when mice were challenged with EBV containing the lytic gene, development of LPD was enhanced. These results indicate that lytic gene expression contributes to EBV-associated LPD.
"Our results suggest that the decreased ability of immunosuppressed hosts to control the lytic form of EBV may promote the development of LPD not only by allowing enhanced horizontal transmission of the virus but also by increasing the number of lytically infected tumor cells," say the researchers.
(G.K. Hong, M.L. Gulley, W.H. Feng, H.J. Delecluse, E. Holley-Guthrie, S.C. Kenney. 2005. Epstein-Barr virus lytic infection contributes to lymphoproliferative disease in a SCID mouse model. Journal of Virology, 79. 22: 13993-14003.)
New Study Suggests Human Papillomavirus Could be Spread Through Blood
Potentially transmissible human papillomavirus DNA has been identified in human blood cells suggesting that the virus, traditionally thought to be sexually transmitted, could also be spread through blood products. Researchers from the National Institutes of Health report their findings in the November 2005 issue of the Journal of Clinical Microbiology.
Human papillomavirus (HPV) is most commonly recognized as a sexually transmitted disease that can cause genital warts as well as cervical cancer. It had been widely accepted that HPVs could not be disseminated through blood. However, the successful experimental transmission of bovine papillomavirus through blood several years ago suggested that might not be the case.
In the study researchers examined HPV DNA in banked, frozen blood cells from pediatric HIV patients and fresh blood cells from healthy donors. Results showed that eight HIV patient samples (seven of which acquired HIV through blood transfusions) and three healthy donor samples were positive for two subgroups of the HPV type 16 genome and that the DNA could exist in a transmissible form.
"Peripheral blood mononuclear cells (PBMCs) might serve as a source of HPV in the infection of epithelial cells and contribute to their nonsexual spread," say the researchers. "However, additional work is needed to confirm this as a possible mode of HPV transmission."
(S. Bodaghi, L.V. Wood, G. Roby, C. Ryder, S.M. Steinberg, Z.M. Zheng. 2005. Could human papillomaviruses be spread through blood? Journal of Clinical Microbiology, 43. 11: 5428-5434.)
New Gene Identified for Antiviral Activity
Researchers have identified a gene in mice capable of producing an innate antiviral response to infection. Their findings appear in the November 2005 issue of the Journal of Virology.
The innate immune response, largely composed of the alpha/beta interferon system, is the first defense against controlling viral infections. These interferons are produced in response to viral infection and stimulate specific genes to produce antiviral compounds. These interferon-stimulated genes (ISGs) are responsible for many of the bodies' innate antiviral activities, but there are still some effects yet to be explained by the genes already identified.
In the study researchers used a modified Sindbis virus to express selected ISG responses in mice and looked for an attenuated infection. Through this approach they identified the interferon-stimulated gene 15 (ISG15) as having antiviral activity, protecting mice against mortality and decreasing viral replication in multiple organs.
"We show that expression of ISG15 in INF-á/Ã¢R mice attenuates Sindbis virus infection, providing in vivo evidence that ISG15 can function as an antiviral molecule," say the researchers.
(D.J. Lenschow, N.V. Giannakopoulos, L.J. Gunn, C. Johnston, A.K. O'Guin, R.E. Schmidt, B. Levine, H.W. Virgin IV. 2005. Identification of interferon-stimulated gene 15 as an antiviral molecule during Sindbis virus infection in vivo. Journal of Virology, 79. 22: 13974-13983.)
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