Chapter 30 : Molecular Detection and Characterization of Human Immunodeficiency Virus Type 1

Abstract:

AIDS was first described in clinical terms in the United States in 1981, and in 1983, the cause was determined to be infection with a transmittable human retrovirus, eventually named human immunodeficiency virus type 1 (HIV-1). Globally, an estimated 35.3 (32.2 to 38.8) million people were living with HIV in 2012, with 2.3 (1.9 to 2.7) million new HIV infections globally, and 1.6 (1.4 to 1.9) million AIDS deaths in 2012 (http://www.unaids.org/sites/default/files/en/media/unaids/contentassets/documents/epidemiology/2013/gr2013/UNAIDS_Global_Report_2013_en.pdf). This pandemic has highlighted the utility of laboratory diagnostics and its relevance to patient care and treatment monitoring. The concern for transmission via blood products motivated the development of an antibody test in 1985 (1). The current versions of these enzyme-linked immunoabsorbent assays detect IgG seroconversion within a median of 3 to 4 weeks after infection (2). Antiretroviral therapy (ART) came into use, starting with AZT monotherapy, in 1985, and eventually the available number and classes of drugs expanded, which led to a better understanding of viral dynamics. Currently, the standard for managing HIV-1 infected individuals is combination therapy with three or more drugs (http://aidsinfo.nih.gov/guidelines/html/1/adult-and-adolescent-arv-guidelines/0). During this phase of active drug development, viral load testing became the standard of care for managing response to therapy. With advances in therapy, long-term (years) suppression of viral load became possible, but selective drug pressure eventually led to drug resistance. The use of genotypic and occasionally phenotypic resistance testing to accurately direct changes in nucleotides that imply resistance to drug therapy is routine in HIV clinical practice. This chapter will focus on the available molecular tests for diagnosis, monitoring, and management of HIV-1 infected individuals.