Virus-Host Gene Interactions Define HIV-1 Disease Progression

• Type of Material: Article
• Authors: Daniela C. Monaco, Emory University; Zachary Ende, Emory University; Eric Hunter, Emory University
• Language: English
• Date: 2017-01-01
• Publisher: Springer Verlag (Germany)
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © Springer International Publishing AG 2017.
• Final Published Version (URL): http://dx.doi.org/10.1007/82_2017_33
• Title of Journal or Parent Work: Current Topics in Microbiology and Immunology
• ISSN: 0070-217X
• Volume: 407
• Start Page: 31
• End Page: 63
• Keywords: HETEROSEXUAL TRANSMISSION; Oncology; Science & Technology; VIRAL-LOAD; MUCOSAL HOMING RECEPTOR; ESCAPE MUTATIONS; Genetics & Heredity; REPLICATION CAPACITY; T-LYMPHOCYTE RESPONSE; INFECTIOUS MOLECULAR CLONES; SIMIAN-IMMUNODEFICIENCY-VIRUS; Virology; TRANSMITTED FOUNDER HIV-1; Life Sciences & Biomedicine; TYPE-1 INFECTION
• Research Categories: Biology, Virology; Health Sciences, Oncology; Biology, Genetics

Abstract

In this chapter, we will review recent research on the virology of HIV-1 transmission and the impact of the transmitted virus genotype on subsequent disease progression. In most instances of HIV-1 sexual transmission, a single genetic variant, or a very limited number of variants from the diverse viral quasi-species present in the transmitting partner establishes systemic infection. Transmission involves both stochastic and selective processes, such that in general a minority variant in the donor is transmitted. While there is clear evidence for selection, the biological properties that mediate transmission remain incompletely defined. Nevertheless, the genotype of the transmitted founder virus, which reflects prior exposure to and escape from host immune responses, clearly influences disease progression. Some escape mutations impact replicative capacity, while others effectively cloak the virus from the newly infected host’s immune response by preventing recognition. It is the balance between the impact of escape mutations on viral fitness and susceptibility to the host immunogenetics that defines HIV-1 disease progression.