Productive HIV infection requires completion of all the steps of the replication cycle, the success of which largely relying on the multiple interactions established by viral proteins with cellular partners. Indeed, cellular and viral fates are intertwined and this interplay may involve rerouting of cellular factors/pathways to the benefit of the viral life cycle. To gain a foothold into host cells, HIV has to take advantage of available cellular factories and overcome the numerous potential blocks opposed to its replication while ensuring cellular survival. Viral auxiliary proteins are a perfect paradigm to illustrate the complexity of the relationship between HIV and its host. Although these accessory proteins are mostly unnecessary for viral replication in permissive cells in vitro, they play a crucial role in regulating viral spread ex vivo in non-permissive cells and in vivo in hosts. Most accessory proteins are pleiotropic and instrumental in the counteraction of restriction factors and proteins involved in innate immune response.
Several proteins of the “intrinsic” immune system that detect the presence of the assailant and initiate a subsequent immune response, as well as restriction factors that are directly devoted to arresting the replication cycle at precise steps have been characterized. Despite the numerous cellular mechanisms dedicated to preventing viral replication, HIV is able to efficiently replicate in humans. Indeed, as a master regulator of cellular machineries and processes, not only has HIV evolved strategies to avoid triggering of pattern recognition receptors, but HIV has also elaborated ways to counteract host restriction factors, thereby overcoming the hurdles that oppose efficient replication.
This review collection is dedicated to the manipulation of host cells by HIV-1 and HIV-2 , with a particular focus on viral accessory proteins.
Key topics include but are not restricted to:
- Regulation of Host cell permissiveness by Viral auxiliary proteins
This topic may include reviews of how HIV and SIV modulate the intracellular environment in favor of the early events of the viral life cycle. For example, the main associated Nef-function, hijacking of the endocytic pathways, and its consequences on host cells permissiveness may be explored. In addition, the cellular pathways diverted by the virus to render the host cell a fertile ground for viral infection may be reviewed, such as counteraction of restriction factors and avoiding of intrinsic immunity triggering. The contribution of viral auxiliary proteins independently and concertedly may be addressed.
- Regulation of viral production and spread by viral auxiliary proteins
This topic should address the late events of the viral life cycle. This may include the many mechanisms by which the virus increases host cell survival, such as the blocking of apoptotic signaling. The mechanisms underlying the counteraction of restriction factors and subversion of intrinsic immune signaling should also be explored. The contribution of viral auxiliary proteins independently and concertedly may be addressed.
- Reviews exploring the functions of viral auxiliary proteins will be included in this collection, specifically Nef, Vpu, Vpr, Vif andVpx.
Productive HIV infection requires completion of all the steps of the replication cycle, the success of which largely relying on the multiple interactions established by viral proteins with cellular partners. Indeed, cellular and viral fates are intertwined and this interplay may involve rerouting of cellular factors/pathways to the benefit of the viral life cycle. To gain a foothold into host cells, HIV has to take advantage of available cellular factories and overcome the numerous potential blocks opposed to its replication while ensuring cellular survival. Viral auxiliary proteins are a perfect paradigm to illustrate the complexity of the relationship between HIV and its host. Although these accessory proteins are mostly unnecessary for viral replication in permissive cells in vitro, they play a crucial role in regulating viral spread ex vivo in non-permissive cells and in vivo in hosts. Most accessory proteins are pleiotropic and instrumental in the counteraction of restriction factors and proteins involved in innate immune response.
Several proteins of the “intrinsic” immune system that detect the presence of the assailant and initiate a subsequent immune response, as well as restriction factors that are directly devoted to arresting the replication cycle at precise steps have been characterized. Despite the numerous cellular mechanisms dedicated to preventing viral replication, HIV is able to efficiently replicate in humans. Indeed, as a master regulator of cellular machineries and processes, not only has HIV evolved strategies to avoid triggering of pattern recognition receptors, but HIV has also elaborated ways to counteract host restriction factors, thereby overcoming the hurdles that oppose efficient replication.
This review collection is dedicated to the manipulation of host cells by HIV-1 and HIV-2 , with a particular focus on viral accessory proteins.
Key topics include but are not restricted to:
- Regulation of Host cell permissiveness by Viral auxiliary proteins
This topic may include reviews of how HIV and SIV modulate the intracellular environment in favor of the early events of the viral life cycle. For example, the main associated Nef-function, hijacking of the endocytic pathways, and its consequences on host cells permissiveness may be explored. In addition, the cellular pathways diverted by the virus to render the host cell a fertile ground for viral infection may be reviewed, such as counteraction of restriction factors and avoiding of intrinsic immunity triggering. The contribution of viral auxiliary proteins independently and concertedly may be addressed.
- Regulation of viral production and spread by viral auxiliary proteins
This topic should address the late events of the viral life cycle. This may include the many mechanisms by which the virus increases host cell survival, such as the blocking of apoptotic signaling. The mechanisms underlying the counteraction of restriction factors and subversion of intrinsic immune signaling should also be explored. The contribution of viral auxiliary proteins independently and concertedly may be addressed.
- Reviews exploring the functions of viral auxiliary proteins will be included in this collection, specifically Nef, Vpu, Vpr, Vif andVpx.