The disease that came to be known as acquired immunodeficiency syndrome (AIDS) was first reported in 1981 in cohort of young homosexual males affected by Pneumocystis carinii (now jiroveci) pneumonia.1 The retrovirus now known as human immunodeficiency virus (HIV) was isolated in 1983 and determined to be the cause of AIDS.2 Disease progression of HIV ultimately leads to the development of AIDS. Diagnosis of AIDS is based on the presence of an AIDS-defining condition or specific laboratory data as detailed later in the chapter.
Since 1981, 25 million deaths have been attributed to AIDS. Globally, there were an estimated 36 million people living with HIV in 2007 with an estimated 2.7 million new infections occurring annually.3 At the end of 2006, an estimated 1.1 million persons in the United States (US) were living with HIV infection, with an estimated 21% undiagnosed. Fifty-six thousand new (HIV or AIDS) infections were diagnosed in the United States for 2006.4
HIV infects cells that express CD4 receptors (T-helper lymphocytes, monocytes, macrophages, dendritic cells, and brain microglia). The glycoprotein (gp) 160 on HIV interacts with CD4 and binds via the gp120 subunit of gp160. HIV then binds chemokine coreceptors (CCR5 and CXCR4). CD4 and coreceptor attachment of HIV to the target cell promotes membrane fusion via gp 41, a subunit of gp160, and then internalization of HIV genetic material and enzymes to begin the replication process. The virus is uncoated and reverse transcription of viral RNA to DNA begins via the enzymereverse transcriptase. Once the DNA is transcribed, the proviral DNA is integrated in host cell DNA via the enzyme integrase. Once integrated, the transcription of DNA occurs within the nucleus causing nuclear release of viral genomic RNA and mRNA. Translation of the RNA and mRNA into viral proteins occurs and are then assembled by viral protease and packaged into a budding virion. Protease is responsible for cleaving a precursor polypeptide (gag-pol) into functional proteins that are necessary to produce mature, infectious virus. Once mature, the virus will infect other susceptible cells causing ongoing immune system destruction with approximately 10 billion new viruses produced each day. The rapid and complex HIV replication process is prone to mistakes causing numerous mutations, which allows the virus to evade the immune response and allows antiretroviral resistance to evolve.5
There are three primary modes of transmission for HIV: sexual (vaginal, anal, or oral), parenteral, and perinatal. Once infected, 40% to 90% of patients will have an acute retroviral syndrome which closely mimics a mononucleosis-like illness with fever, pharyngitis, lymphadenopathy, weight loss, night sweats, diarrhea, and nausea. Symptoms typically occur 2 to 6 weeks after exposure and can persist for 2 to 10 weeks. Acute infection is associated with a high viral load and a decrease in CD4 cells, but after ...