Running head: VIRAL INFECTIOUS DISEASE: HIV
Viral Infectious Disease: HIV
Acquired immunodeficiency syndrome (AIDS) was first described in the early 1980s, although it was known by other names for several years. In its 30 years of existence, this disease, caused by the human immunodeficiency virus (HIV), has become pandemic. In the United States, it initially appeared to affect primarily gay men; however, it is now known to occur worldwide, and among all populations. In this paper, the structure of the HIV virus will be discussed as well as its infectious cycle and pathology. In addition, prospects for HIV vaccine will be briefly examined as well as the potential for antiviral drugs.
Viral Infectious Disease: HIV
The epidemic of HIV disease and AIDS is now well into its third decade. It has garnered more attention than any new disease to appear in recent history, and it continues to spread. Acquired immunodeficiency syndrome, better known as AIDS, threatens significant portions of the human population. Although the 1990s have witnessed major advances in treatment, HIV infection remains an ultimately fatal disorder.
Structure of HIV
HIV is a typical retrovirus in size and shape. Two antigenic glycoproteins characterize its envelope. The larger glycoprotein, named gp120, is the primary attachment molecule of HIV to four kinds of cells: helper T cells, cells of the macrophages lineage, smooth muscle cells, and dendritic cells (Huang, Lam, Acharya, Tang, Xiang, et al., 2007). Its antigenicity changes during the course of prolonged infection, making an effective antibody response against it difficult (Huang, Lam, Acharya, Tang, Xiang, et al., 2007). The smaller glycoprotein, gp41, promotes fusion of the viral envelope to a target cell and the HIV virus releases its ssRNA genome from the capsid into the cell’s cytoplasm (Zhou, Lu, Tan, Jiang & Chen, 2011). The effects of these structural characteristics – antigenic variability and the ability to fuse with host cells – interfere with clearance of HIV from a patient (Kwong, Wyatt, Robinson, et al. (1998).
The infectious cycle of HIV infection
AIDS develops as the end result of long-term infection with one of two closely related viruses, HIV-1 and the less common HIV-2 (Porter & Kaplan, 2004). The two viruses are very similar structurally and cause identical clinical manifestations (Frahm & Brander, 2007). They are both single-stranded RNA retroviruses, so named because they can transcribe their viral RNA into DNA (Krasinski, 1994). For HIV infection to occur, the virus must be absorbed into the bloodstream. Then surface protein on the virus outer wall, or envelope, bind to receptors on the outer surface of CD4+ cells, including T-lymphocytes (Huang, Lam, Acharya, Tang, Xiang, et al., 2007). After attachment, the viral RNA enters the host cell and is transcribed by a viral reverse transcriptase enzyme into double-stranded DNA( Kwong et al, 1998). This viral-encoded DNA is transported into the cell nucleus, where it is incorporated into the host-cell DNA. The viral DNA then directs the host cell to produce HIV-specific proteins (Frahm & Brander, 2007). These proteins, according to Frahm & Brander (2007) must be cut, or cleaved, by another viral protein, called a protease, into segments. The segments are then assembled into infectious viruses, which either bud off from the host cell or are released on cell death (Porter & Kaplan, 2004). The mechanism of viral replication is important to understand because approaches to treatment are based on the viral life cycle (Porter & Kaplan, 2004).
HIV infection inflicts damage to the host immune system through the progressive loss of CD4+ T-lymphocytes (Porter & Kaplan, 2004). The lymphocytes, termed helper/suppressor cells, are critical in modulating the normal immune response. At first, the body’s immune response keeps up with the active viral...
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