TY - JOUR
T1 - The Vif of human immunodeficiency virus type 1 (HIV-1)
T2 - Enigmas and solutions
AU - Baraz, Lea
AU - Kotler, Moshe
PY - 2004
Y1 - 2004
N2 - HIV-1 and other complex retroviruses express six auxiliary genes in addition to the canonical retroviral genes, gag, pol and env. Vif (virion infectivity factor) protein is absolutely essential for productive HIV-1 infection of peripheral blood lymphocytes and macrophages, the two major HIV-1 target cells in vivo. However, Vif is not required for production of infectious particles in several human cell lines. In spite of the prominent phenotype of Vif mutations, the mechanism of its action remains unknown. During the last decade several models were suggested to explain the mechanism of Vif activity. One view holds that Vif is active in virions after budding or after entry into target cells during the early stages of HIV-1 replications. The second view places the action of Vif at the late stage of HIV-1 replication in virus producing cells, which affects the production of infectious virus. According to this view, Vif either compensates the cell factor required for production of infectious virus, or alternatively, it neutralizes a cell factor, which prevents the production of infectious particles in these cells. This review is addressed to summarize the models envisioned to explain Vif activities. The findings described here, that Vif interacts with viral and cellular components, elaborates the importance of Vif as a novel target for developing anti HIV-1 drugs.
AB - HIV-1 and other complex retroviruses express six auxiliary genes in addition to the canonical retroviral genes, gag, pol and env. Vif (virion infectivity factor) protein is absolutely essential for productive HIV-1 infection of peripheral blood lymphocytes and macrophages, the two major HIV-1 target cells in vivo. However, Vif is not required for production of infectious particles in several human cell lines. In spite of the prominent phenotype of Vif mutations, the mechanism of its action remains unknown. During the last decade several models were suggested to explain the mechanism of Vif activity. One view holds that Vif is active in virions after budding or after entry into target cells during the early stages of HIV-1 replications. The second view places the action of Vif at the late stage of HIV-1 replication in virus producing cells, which affects the production of infectious virus. According to this view, Vif either compensates the cell factor required for production of infectious virus, or alternatively, it neutralizes a cell factor, which prevents the production of infectious particles in these cells. This review is addressed to summarize the models envisioned to explain Vif activities. The findings described here, that Vif interacts with viral and cellular components, elaborates the importance of Vif as a novel target for developing anti HIV-1 drugs.
KW - Cellular anti-HIV-1 factor
KW - Drug resistance
KW - HIV-1
KW - HIV-1 protease
KW - Peptide-mapping
KW - Protease inhibitors
KW - Vif
UR - http://www.scopus.com/inward/record.url?scp=1642544665&partnerID=8YFLogxK
U2 - 10.2174/0929867043456124
DO - 10.2174/0929867043456124
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C2 - 14754418
AN - SCOPUS:1642544665
SN - 0929-8673
VL - 11
SP - 221
EP - 231
JO - Current Medicinal Chemistry
JF - Current Medicinal Chemistry
IS - 2
ER -