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1.  Novel roles of the picornaviral 3D polymerase in viral pathogenesis 
Advances in virology  2010;2010:368068.
The RNA-dependent RNA-polymerase, 3Dpol, is an essential component in the picornavirus genome for the replication of single stranded RNA. However, transgenic expression of 3Dpol in mice has antiviral effects. Here we discuss the structure and function of 3Dpol during picornavirus replication, we review the evidence and consequence of a host immune response to epitopes in 3Dpol after picornavirus infection, highlight data showing the antiviral effects of transgenic 3Dpol from Theiler’s murine encephalomyelitis virus (TMEV), and discuss potential mechanisms by which 3Dpol is causing this antiviral effect in mice.
doi:10.1155/2010/368068
PMCID: PMC2897181  PMID: 20625447
2.  Towards Inhibition of Vif-APOBEC3G Interaction: Which Protein to Target? 
Advances in Virology  2010;2010:649315.
APOBEC proteins appeared in the cellular battle against HIV-1 as part of intrinsic cellular immunity. The antiretroviral activity of some of these proteins is overtaken by the action of HIV-1 Viral Infectivity Factor (Vif) protein. Since the discovery of APOBEC3G (A3G) as an antiviral factor, many advances have been made to understand its mechanism of action in the cell and how Vif acts in order to counteract its activity. The mainstream concept is that Vif overcomes the innate antiviral activity of A3G by direct protein binding and promoting its degradation via the cellular ubiquitin/proteasomal pathway. Vif may also inhibit A3G through mechanisms independent of proteasomal degradation. Binding of Vif to A3G is essential for its degradation since disruption of this interaction is predicted to stimulate intracellular antiviral immunity. In this paper we will discuss the different binding partners between both proteins as one of the major challenges for the development of new antiviral drugs.
doi:10.1155/2010/649315
PMCID: PMC3275931  PMID: 22347227
3.  Cells in Dengue Virus Infection In Vivo 
Advances in Virology  2010;2010:164878.
Dengue has been recognized as one of the most important vector-borne emerging infectious diseases globally. Though dengue normally causes a self-limiting infection, some patients may develop a life-threatening illness, dengue hemorrhagic fever (DHF)/dengue shock syndrome (DSS). The reason why DHF/DSS occurs in certain individuals is unclear. Studies in the endemic regions suggest that the preexisting antibodies are a risk factor for DHF/DSS. Viremia and thrombocytopenia are the key clinical features of dengue virus infection in patients. The amounts of virus circulating in patients are highly correlated with severe dengue disease, DHF/DSS. Also, the disturbance, mainly a transient depression, of hematological cells is a critical clinical finding in acute dengue patients. However, the cells responsible for the dengue viremia are unresolved in spite of the intensive efforts been made. Dengue virus appears to replicate and proliferate in many adapted cell lines, but these in vitro properties are extremely difficult to be reproduced in primary cells or in vivo. This paper summarizes reports on the permissive cells in vitro and in vivo and suggests a hematological cell lineage for dengue virus infection in vivo, with the hope that a new focus will shed light on further understanding of the complexities of dengue disease.
doi:10.1155/2010/164878
PMCID: PMC3276057  PMID: 22331984
4.  Novel Roles of the Picornaviral 3D Polymerase in Viral Pathogenesis 
Advances in Virology  2010;2010:368068.
The RNA-dependent RNA-polymerase, 3Dpol, is an essential component in the picornavirus genome for the replication of single stranded RNA. However, transgenic expression of 3Dpol in mice has antiviral effects. Here, we discuss the structure and function of 3Dpol during picornavirus replication, we review the evidence and consequence of a host immune response to epitopes in 3Dpol after picornavirus infection, highlight data showing the antiviral effects of transgenic 3Dpol from Theiler's murine encephalomyelitis virus (TMEV), and discuss potential mechanisms by which 3Dpol is causing this antiviral effect in mice.
doi:10.1155/2010/368068
PMCID: PMC2897181  PMID: 20625447

Results 1-4 (4)