Viral Interference of GB Virus C and Human Immunodeficiency Viruses

In general, infection of a host by multiple pathogens has important clinical implications. In conjunction with HIV, co-infections are associated with a significantly decreased survival probability. Unexpectedly, long-term viremia of the apathogenic GB Virus C (GBV-C) leads to improved survival of GBV-C co-infected HIV patients. However, epidemiological studies cannot prove a causal relationship nor they distinguish whether the observed reduction in HIV associated morbidity and mortality is caused by GBV-C/HIV interference or if GBV-C serves just as a surrogate marker for a robust immune system. Therefore, cell culture experiments were necessary. Indeed, GBV-C inhibits different HIV strains and clades. The underlaying mechanism of HIV suppression is complex. In addition to GBV-C proteins, such as the E2 glycoprotein that possess the ability to inhibit HIV entry or the NS5A protein that may imair later HIV replication steps, GBV-C elicits antibodies that neutralize HIV comparable to the broad reactive human anti-gp41 antibodies 2F5 and 4E10, as well. Taken together a combination of both inhibitory effects present an innovative approach for further drug development and vaccine design.

Autorentext

Susan Jung was born in 1980 in Frankenberg, Germany. She studiedbiology at the Friedrich-Alexander University Erlangen, where shereceived her PhD in Natural Sciences in 2010. Her research at theNational Reference Center for Retroviruses focuses on thepersistence and viral interference of new flaviviruses andimmunodeficiency viruses.