1,721,195 research outputs found
Are three generations of quantitative molecular methods sufficient in medical virology? Brief review
No full textIn the last two decades, development of quantitative molecular methods has characterized the evolution of clinical virology more than any other methodological advancement. Using these methods, a great deal of studies has addressed efficiently in vivo the role of viral load, viral replication activity, and viral transcriptional profiles as correlates of disease outcome and progression, and has highlighted the physio-pathology of important virus diseases of humans. Furthermore, these studies have contributed to a better understanding of virus-host interactions and have sharply revolutionized the research strategies in basic and medical virology. In addition and importantly from a medical point of view, quantitative methods have provided a rationale for the therapeutic intervention and therapy monitoring in medically important viral diseases. Despite the advances in technology and the development of three generations of molecular methods within the last two decades (competitive PCR, real-time PCR, and digital PCR), great challenges still remain for viral testing related not only to standardization, accuracy, and precision, but also to selection of the best molecular targets for clinical use and to the identification of thresholds for risk stratification and therapeutic decisions. Future research directions, novel methods and technical improvements could be important to address these challenges
Anti-HCV monoclonal antibody as a medicament for the therapeutic treatment and prevention of HCV infections
No full text
Human immunodeficiency virus type 1 fitness and tropism: concept, quantification, and clinical relevance
No full textAbstractTwo distinct aspects of human immunodeficiency virus type 1 (HIV-1) biopathology with important implications for the management of treated patients have emerged during the last decade: changes in relative viral fitness, and viral tropism. First, it has been observed that HIV-1 accumulates deleterious mutations leading to drug resistance and different degrees of reduction in relative fitness during antiretroviral therapy (ART). Although the latter normally parallel a failure of ART resulting from selection of resistant mutants, the drop in viral replication capacity may be beneficial for the host. Moreover, specific antiviral compounds aimed at reducing viral fitness could be developed. Analysis of the determinants of viral fitness in highly evolving viral populations has shown that viral extinction may also be obtained by forcing highly dynamic viral populations through increased (lethal) mutagenesis that abolishes viral replication (violation of the error threshold). It could be of great interest in the near future to address this point with strategies specifically planned at the molecular level. Furthermore, diagnostic evaluation limited to the master sequence has low predictive value in rapidly evolving viral populations. These observations, together with the evidence that all of the methodologies currently used for fitness analysis have important limitations, strongly suggest that further research is warranted. This should use highly sensitive and flexible technologies to evaluate viral fitness directly in vivo or ex vivo, not only for the dominant mutants, but also for minority variants. Second, discovery of the two main co-receptors for HIV-1, CCR5 and CXCR4, has led to a better understanding of the interaction of the viral envelope with host cells and to the development of novel therapeutic agents that inhibit viral entry. In this perspective, analysis of HIV-1 tropism has acquired a major diagnostic role
Molecular signatures of hepatitis C virus (HCV)-induced type II mixed cryoglobulinemia (MCII)
Full text linkThe role of hepatitis C virus (HCV) infection in the induction of type II mixed
cryoglobulinemia (MCII) and the possible establishment of related lymphoproliferative
disorders, such as B-cell non-Hodgkin lymphoma (B-NHL), is well ascertained.
However, the molecular pathways involved and the factors predisposing to the
development of these HCV-related extrahepatic complications deserve further
consideration and clarification. To date, several host- and virus-related factors have been
implicated in the progression to MCII, such as the virus-induced expansion of selected
subsets of B-cell clones expressing discrete immunoglobulin variable (IgV) gene
subfamilies, the involvement of complement factors and the specific role of some HCV
proteins. In this review, we will analyze the host and viral factors taking part in the
development of MCII in order to give a general outlook of the molecular mechanisms
implicated
- …
