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Current Research in the Field of Herpesvirology

The field of herpesvirus research has seen important developments in the past year (2007-2008), including associations between herpes simplex virus 2 (HSV-2) and HIV transmission, potential benefits of latent herpesvirus infections, vertical transmission of human herpesvirus 8 (Kaposi sarcoma-associated herpesvirus), the role of specific herpesvirus proteins in evading the host immune response, and the use of human herpesviruses in novel therapeutic strategies.  Below are some of the exciting developments in herpesvirus research. 


“Proportion of new HIV infections attributable to herpes simplex 2 increases over time: simulations of the changing role of sexually transmitted infections in sub-Saharan African HIV epidemics.”  

With the objective of better understanding the role of herpes simplex virus type 2 (HSV-2) and other sexually transmitted infections on the incidence of HIV in sub-Saharan Africa, Freeman et al.  found that, in 4 cities in Kenya, Zambia, Benin, and Cameroon, the number of HIV infections attributable to concurrent HSV-2 infections had risen over time in each of the cities.  Namely, the impact of HSV-2 increased as the epidemic continued, with a lower impact seen in areas with relatively new epidemics and a higher impact in areas with mature epidemics.  The study also found that recurrent HSV-2 lesions were associated with higher rates of HIV transmission than were primary HSV-2 lesions.  Conclusions to be drawn from the study are that HSV-2 infection has a smaller impact at the beginning of an HIV epidemic, due to the fact that HIV infection is confined to specific groups.  Later in the HIV epidemic, when it becomes generalized, the impact of HSV-2 incidence on HIV transmission is much greater.  Thus, interventions to prevent HSV-2 infection may play an important role in HIV prevention.  

Freeman, Esther E., et al.  “Proportion of new HIV infections attributable to herpes simplex 2 increases over time: simulations of the changing role of sexually transmitted infections in sub-Saharan African HIV epidemics.”  Sexually Transmitted Infections.  83 (2007): i17-i24. 


“Herpesvirus latency confers symbiotic protection from bacterial infection.”

In this study by Barton et al., a possible protective mechanism was identified between latent herpesvirus infection and resistance to several bacteria.  Mice infected with murine gammaherpesvirus 68 or murine cytomegalovirus, which closely ressemble Epstein-Barr virus and human cytomegalovirus, showed decreased susceptibility to infection with Listeria monocytogenes and Yersinia pestis.  This increased protection was found to be due to the continuous high rates of antiviral cytokine production, and specifically interferon-gamma production, as well as increased macrophage activation in mice infected with the herpesviruses.  Thus, because innate immune system of these mice was upregulated, causing a protective effect, herpesvirus infection may be considered not only pathogenic, but also partially symbiotic.  

Barton, Erik S., et al.  “Herpesvirus latency confers symbiotic protection from bacterial infection.”  Nature.  447 (2007): 326-329.

 

“Transmission of Kaposi Sarcoma-Associated Herpesvirus Between Mothers and Children in a South African Population.”

Babatyi et al. studied patterns of vertical transmission of Kaposi sarcoma-associated herpesvirus, also known as human herpesvirus 8, in South Africa.  The risk of Kaposi sarcoma-associated herpesvirus (KSHV) was found to be significantly higher in children born to KSHV seropositive mothers, confirming previous hypotheses that KSHV could be transmitted from mother to child.  The study included women both seropositive and seronegative for HIV, and found that, although the rates of KSHV were much higher in women with HIV, the risk of transmission of KSHV in mothers who were HIV positive and HIV negative was not significantly different.  Thus, HIV infection does not seem to have a significant impact on vertical KSHV transmission.   

Malope, Babatyi, et al.  “Transmission of Kaposi Sarcoma-Associated Herpesvirus Between Mothers and Children in a South African Population.”  Journal of Acquired Immune Deficiency Syndromes.  44 (2007):  44:3.

 

“Downregulation of Gamma Interferon Receptor 1 by Kaposi’s Sarcoma-Associated Herpesvirus K3 and K5.” 

In this paper, Qinglin et al. explore viral evasion of the host immune response by examining how Kaposi’s sarcoma-associated herpesvirus (KSHV) interferes with the host’s antiviral interferon (IFN) response.  Specifically, Qinglin et al. found that the K3 and K5 KSHV viral proteins functioned to target the gamma interferon receptor, leaded to decreases in cell-mediated immune pathways.  K3 and K5 have the ability to uniquitinate and ultimately degrade the gamma interferon receptors, leading to a significant decrease in gamma interferon production.  Through this inactivation, KSHV is able to evade the host immune system by inhibiting both cell- and cytokine-mediated immune pathways.  

Li, Qinglin, et al.  “Downregulation of Gamma Interferon Receptor 1 by Kaposi’s Sarcoma-Associated Herpesvirus K3 and K5.”  Journal of Virology.  81 (2007): 2117-2127. 

  

“Viral Interactions in Human Lymphoid Tissue: Human Herpesvirus 7 Suppresses the Replication of CCR5-Tropic Human Immunodeficiency Virus Type 1 via CD4 Modulation.”

Lisco et al. found that human herpesvirus 7 (HHV-7) infection inhibits HIV type 1 replication in human lymphoid tissues.  In lymphoid tissues coinfected with both viruses, HHV-7 can suppress the replication of CCR5-tropic species of HIV-1 through downregulating expression of the shared CD4 receptor on the infected host cell surface.  This decreased CD4 expression results in the resulting suppression of HIV replication.  These findings may have important implications for the progression of HIV-1 in patients concurrently infected with HHV-7, and may provide a new avenue for therapeutic strategies for HIV.    

Lisco, Andrea, et al.  “Viral Interactions in Human Lymphoid Tissue: Human Herpesvirus 7 Suppresses the Replication of CCR5-Tropic Human Immunodeficiency Virus Type 1 via CD4 Modulation.”  Journal of Virology.  81 (2007): 708-717.