This web page was produced as an assignment for an undergraduate course at Davidson College.
Innate Immune Response
The HIV virus relies on its hosts to carry it past their first line of defense for it needs access to various components of the immune system before it can begin its attack. There are a number of ways that the virus can be introduced into a host - sharing needles, exposure to mother's blood during pregnancy, breast milk - but by far, the most prevalent means is sexual contact (Paul, 2003). HIV can spread easily through rectal or vaginal abrasions during intercourse. Upon entering a new host, the viral molecules use the innate immune system against the host to propogate the proliferation.
Two tropisms have been defined for the HIV-1 strain: T-tropic and M-Tropic. M-tropic (macrophage tropic) strains are seen at much higher levels during initial infection than are the T-tropic (T cell trophic) strains, thus macrophages are thought to play a crucial role in the contraction of the virus (Clerici et al, 1999).. The origin of the tropism has been found to be the third variable region (V3) of the gp120 protein (the HIV envelope protein that binds CD-4) (Clerici et al, 1999).
The uptake of virions by macrophages is aided by DC-SIGN which binds gp120, a process which is beneficial to HIV because it aids in the transport of the virus to CD4+ T cells in the periphery (Rubbert et al, 2006). Moreover, HIV is capable of replicating in vacuoles inside the macrophage, thus helping to establish long-term reservoirs (Rubbert et al, 2006). Moreover, the HIV virus is resistant to destruction through complement, although the pathway is allowed to continue to the point of opsonizing the viral particle with C3b (Clerici et al, 1999). This increases the likelihood of macrophages and other APCs phagocytosing the virus so it can begin replicating in their endosomes. Moreover, the M-tropic HIV-1 binds with high affinity for the CCR5 co-receptor that's expression is induced upon maturation of monocytes (Clerici et al, 1999).. Upon successful infection, the virus is able to prevent the macrophages using IL-1 to activate certain T cells (Stine, 1993). The virus is then able to reproduce rapidly inside the macrophages until they are carried to the lymph nodes and transferred to CD4 T cells (Stine, 1993). In this way, the virus uses the host's innate immune response to spread itself to its main target cells.
Clerici, M., et al. 1999. The Relationships Between Cytokines, Complement and HIV Infection. In: Dalgleish, A., Weiss, R., editors. HIV and the New Viruses. 2nd ed. San Diego: Academic Press, 1999.
Paul, William ed. Fundamental Immunology. 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2003.
Rubbert, A., et al . 2006. Pathogenesis of HIV-1 Infection. In: Hoffmann, C., Rockstroh, J., Kamps, B., editors. HIV Medicine 2006. Flying Publisher. <http://www.hivmedicine.com/index.htm>. (5 May 2007).
Stine, Gerald. Acquired Immune Deficiency Syndrome. New Jersey: Prentice-Hall Inc, 1993.