Disease relevance of Virus Replication

• The Vif gene of HIV-1 blocks this host restriction and so allows virus replication [1].
• Nitric oxide inhibits hepatitis B virus replication in the livers of transgenic mice [2].
• These data show that patients treated with long-term levamisole therapy have a tendency toward normalization of aminotransferase activities and suppression of hepatitis B virus replication, suggesting that the drug may be of benefit in chronic hepatitis B e antigen-positive hepatitis [3].
• These findings underscore the importance of HCF-1 to herpes simplex virus replication and VP16 transactivation [4].
• Viral burden (i.e., HIV DNA copies per 10(6) mononuclear cells) and virus replication in mononuclear cells isolated from peripheral blood and lymph node and plasma viremia were determined by semiquantitative polymerase chain reaction assays [5].

High impact information on Virus Replication

• The similarity of this mouse model to human AIDS, particularly pediatric AIDS, suggests that Nef may play a critical role in human AIDS, independently of its role in virus replication [6].
• The HIV-1 Tat protein is a potent trans-activator essential for virus replication [7].
• Thus, an essential function of Gam1 during virus replication is to activate host heat-shock responses with hsp40 as a primary target [8].
• Phosphorylation of eukaryotic initiation factor 2alpha (eIF2alpha) blocks translation initiation of both cellular and viral mRNA, inhibiting virus replication [9].
• Here, we identify that host factors allow increased virus replication and cytokine production, providing a mechanism for understanding the severity of virus disease in CF [10].

Chemical compound and disease context of Virus Replication

• BACKGROUND & AIMS: Lamivudine inhibits hepatitis B virus replication [11].
• Inhibition of hepatitis B virus replication by vidarabine monophosphate conjugated with lactosaminated serum albumin [12].
• In contrast, introduction of both gag MA and Vpr mutations in HIV-1 attenuated nuclear localization of viral nucleic acids in nondividing cells and virus replication in monocyte-derived macrophages [13].
• Substitution of the myristoyl-acceptor glycine with alanine, in a functional clone of HIV-1, eliminates virus replication [14].
• These results indicate that ribavirin suppresses hepatitis B virus replication, although its effect is less than that of interferon, and that it may be useful as adjunctive therapy for chronic hepatitis B.(ABSTRACT TRUNCATED AT 250 WORDS)[15]

Biological context of Virus Replication

• In the case of LCMV-immune versus naive mice challenged with VV, there was an enhanced early recruitment of memory phenotype interferon (IFN) gamma-secreting CD4(+) and CD8(+) cells into the peritoneal cavity and increased IFN-gamma levels in this initial site of virus replication [16].
• The expression of two heat-inducible genes encoding HSP70 and polyubiquitin was induced coordinately with the onset of virus replication and the down-regulation of two other genes encoding lipoxygenase and heat shock cognate protein [17].
• Mutations that alter the sequence of the sites normally used for cleavage of the major capsid protein p24 from the capsid precursor alter virion morphogenesis and prevent virus replication [18].
• Plasmid expressing AS IL-4 DNA was also effective in abrogating virus replication in macrophage cultures [19].
• To address the role of p53 in virus replication, amino acid substitutions were introduced into the NH(2)-terminal portion of p53, replacing residues 24-28 with the corresponding sequence of the human p53-homologue p73 [20].

Anatomical context of Virus Replication

• In a comparative study, 2 microM GEM91 was as effective as 5 microM 3'-azido-3'-deoxythymidine in blocking virus replication during the 28-day treatment of an HIV-1-infected T-cell line [21].
• Mutations in the gag, pol, env, and tat regions precluded virus replication and cytopathology in lymphoid cells [22].
• We demonstrate that significantly increased (P < 0.02) activation of ERK MAPK, typically associated with anti-apoptotic and neuroprotective pathways, occurs predominantly in astrocytes and immediately precedes suppression of virus replication and macrophage activation that occur after acute infection [23].
• The data further imply that IFN-gamma plays a crucial role in pathogenesis by regulating the balance between virus replication in oligodendrocytes, CD8(+) T cell effector function, and demyelination [24].
• These data suggest that although perforin-dependent CTL control virus replication within astrocytes and microglia, which constitute the majority of infected CNS cells, IFN-gamma is critical for control of viral replication in oligodendroglia [25].

Associations of Virus Replication with chemical compounds

• However, virus replication is required for M-protein appearance [26].
• We evaluated cell response by measuring virus replication, [3H]thymidine incorporation, 2',5'-oligoadenylate synthetase activation, and class I antigen induction [27].
• Cholesterol-depleted cells were unaltered in their ability to bind, internalize, and acidify virus, but were blocked in SFV fusion and subsequent virus replication [28].
• Two such Fabs, which exhibited high binding affinity for RSV F glycoprotein (a major protective antigen), were evaluated for therapeutic efficacy in infected mice just before or at the time of peak virus replication in the lungs [29].
• Satisfactory treatment of the disease can be accomplished with ganciclovir or foscarnet, although these agents only suppress virus replication [30].

Gene context of Virus Replication

• The data also suggest that sor influences virus replication at a novel, post-translational stage and that its action is independent of the regulatory genes tat and trs [31].
• The ability of ced-3 and ced-4 alleles to restrict virus replication is correlated with their cell-killing activities [32].
• Virus replication is enhanced in HDAC6-depleted cells, demonstrating HDAC6 is an essential component of innate antiviral immunity [33].
• Treatment of cells with TNF-alpha in the presence of ZVAD caused increased expression of TNF-alpha and induced enhanced virus replication [34].
• Moreover, expression of the IRF9-STAT2 fusion can recapitulate the type I IFN biological response, producing a cellular antiviral state that protects cells from virus-induced cytopathic effects and inhibits virus replication [35].

Analytical, diagnostic and therapeutic context of Virus Replication

• Immunosuppression by Moloney leukemia virus: lack of correlation between virus replication and the immunosuppressive effect [36].
• L-735,524 is a potent inhibitor of virus replication in cell culture and inhibits the protease-mediated cleavage of the viral precursor polyproteins that results in the production of noninfectious progeny viral particles [37].
• Each of the five subjects with new resistant mutants had evidence of some residual virus replication during highly active antiretroviral therapy (HAART), based on transient episodes of plasma HIV-1 RNA > 50 copies/ml and virus env gene sequence changes [38].
• A tale of two strands: reverse-transcriptase polymerase chain reaction detection of hepatitis C virus replication [39].
• Cell blastogenesis and virus replication did not occur in the purified T-cell cultures incubated with IL-2 alone [40].

References