Báo cáo y học: Intracellular immunity to HIV-1: newly defined retroviral battles inside infected cells

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Báo cáo y học: "Intracellular immunity to HIV-1: newly defined retroviral battles inside infected cells"Retrovirology BioMed Central Open AccessReviewIntracellular immunity to HIV-1: newly defined retroviral battlesinside infected cellsYong-Hui Zheng* and B Matija Peterlin*Address: Departments of Medicine, Microbiology and Immunology, Rosalind Russell Arthritis Research Center, University of California, SanFrancisco, San Francisco, CA, 94143-0703, USAEmail: Yong-Hui Zheng* - yonghui@itsa.ucsf.edu; B Matija Peterlin* - matija@itsa.ucsf.edu* Corresponding authorsPublished: 13 April 2005 Received: 24 February 2005 Accepted: 13 April 2005Retrovirology 2005, 2:25 doi:10.1186/1742-4690-2-25This article is available from: http://www.retrovirology.com/content/2/1/25© 2005 Zheng and Peterlin; licensee BioMed Central Ltd.This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0),which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Studies of the human immunodeficiency virus type 1 (HIV-1) continue to enrich eukaryotic biology and immunology. Recent advances have defined factors that function after viral entry and prevent the replication of proviruses in the infected cell. Some of these attack directly viral structures whereas others edit viral genetic material during reverse transcription. Together, they provide strong and immediate intracellular immunity against incoming pathogens. These processes also offer a tantalizing glimpse at basic cellular mechanisms that might restrict the movement of mobile genetic elements and protect the genome. 3B, 3F and 3G (APOBEC3B, APOBEC3F and APOBEC3GBackgroundAlthough it is highly pathogenic in humans, HIV-1 cannot or A3B, A3F and A3G), which collectively inactivate sev-replicate in most other species [1]. This tropism is deter- eral retroviruses including HIV-1, simian immunodefi-mined primarily by whether host cells express the ciency virus (SIV), hepatitis B virus and some mouserequired cofactors. For example, by lacking a functional mobile genetic elements [3-7]. This review highlightsreceptor and appropriate transcriptional machinery, these recent developments and mentions briefly addi-mouse cells do not support infection by HIV-1. Thus, the tional potential blocks to retroviral replication.organism resists the pathogen via a cell-based incompati-bility. However, a pathogen can also be restricted by the Interference and Restrictionpresence of dominant inhibitory factors. They attack the Let us begin with some definitions and historical perspec-incoming virus directly and block its integration into the tives. Viral interference refers to the situation when cells,host genome. This situation also pertains to HIV-1 in which are chronically infected with one virus or containmouse cells and represents true intracellular immunity. endogenous retroviruses, resist superinfection by otherImportantly, this host response is more rapid than either viruses bearing envelopes with a similar target specificity.traditional innate or adaptive immunity and can prevent This block usually results from the loss of the appropriatethe establishment of the infection. receptor on the cell surface. A good example of this inter- ference is the Friend virus susceptibility factor 4 (Fv4),Recent advances in our understanding of intracellular also known as Akvr-1, which controls the susceptibility ofimmunity have identified two different proteins, the tri- mice to infection by ecotropic but not other murine leuke-partite motif protein 5α (TRIM5α) [2] and the apolipo- mia viruses (MLVs) [8]. This gene is located on mouseprotein B mRNA-editing enzyme catalytic-polypeptides ...