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The authors of a systematic review and meta-analysis conclude that the benefit of convalescent plasma (CP) in the treatment of COVID-19 is limited. Among other systematic reviews, only one found an indication of benefit of CP. However, a meta-analysis needs a focused and meaningful clinical question and should include studies which are designed to test a reasonable hypothesis. Clinical trials to support the licensing of medicines should aim to define as exactly as possible the investigational drug and target disease. In the case of COVID-19, trial details (e.g., duration, stage and severity of disease, and antibody content and dose of CP) are quite heterogeneous. The so far available evidence suggests that the hypothesis should be sharpened as to treat COVID -19 patients at risk for developing severe disease as early enough with a sufficiently high dose of specific antibodies. It has been demonstrated that such an approach is feasible, and the lack of an independent reproduction by further trials with a really comparable design can probably not be compensated by compiling all available, heterogenous trials, even with the best methodology of a systematic review and meta-analysis. Though the COVID-19 pandemic appears to be fading, we should not neglect the search for effective prevention and treatments, given the still high death toll of COVID-19. Monoclonal antibodies were found effective in the early phase of the pandemic; however, due to new variants of SARS-COV2 undermining their efficacy they are no longer recommended by the current NIH guidelines. CP can provide a spectrum of polyclonal antibodies in close timely and regional connection to the particular prevalent virus variant. It would be extremely valuable to obtain a solid scientific foundation for the principle of target specific and temporarily adapted passive immunization, which could be a fast and flexible instrument also in future outbreaks of novel pathogens. [ABSTRACT FROM AUTHOR]

Coinfections with hepatitis B virus (HBV) and HIV are very frequent. Although HBV is a DNA virus, it replicates via reverse transcription like HIV. Structural similarities between the enzymatic pocket of the HBV DNA polymerase and HIV-1 reverse transcriptase are the basis that certain drugs inhibit both enzymes and thus the replication of both viruses. HBV components increase the pathogenic action of HIV and vice versa directly by certain proteins like HBsAg in the case of HBV and HIV-encoded Tat and Vpr and by disturbing the cytokine balance in affected cells. Antiretroviral therapy is highly beneficial for HIV/HBV-coinfected patients, but carries the risk of drug-induced resistance development and hepatotoxicity. Even with restoration of the immune capacity, signs of hepatic inflammation may develop even after 10 years of treatment. © 2014 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

HIV-1 is a chimpanzee virus which was transmitted to humans by several zoonotic events resulting in infection with HIV-1 groups M-P, and in parallel transmission events from sooty mangabey monkey viruses leading to infections with HIV-2 groups A-H. Both viruses have circulated in the human population for about 80 years. In the infected patient, HIV mutates, and by elimination of some of the viruses by the action of the immune system individual quasispecies are formed. Along with the selection of the fittest viruses, mutation and recombination after superinfection with HIV from different groups or subtypes have resulted in the diversity of their patterns of geographic distribution. Despite the high variability observed, some essential parts of the HIV genome are highly conserved. Viral diversity is further facilitated in some parts of the HIV genome by drug selection pressure and may also be enhanced by different genetic factors, including HLA in patients from different regions of the world. Viral and human genetic factors influence pathogenesis. Viral genetic factors are proteins such as Tat, Vif and Rev. Human genetic factors associated with a better clinical outcome are proteins such as APOBEC, langerin, tetherin and chemokine receptor 5 (CCR5) and HLA B27, B57, DRB1*1303, KIR and PARD3B. Copyright © 2012 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Antiretroviral drug resistance is mostly linked to a complex interaction of several amino acids with variable importance or a single amino acid. To facilitate the interpretation of observed mutation patterns, hospital university centers have developed several interpretation systems. All the currently available interpretation algorithms evolved, are being continuously updated and have been improved during the last decade. Some discrepancies are still evident that are partially smoothened by link of the individual programs with other systems. After the interpretation of HIV-1 group M subtype B mutations, a refined algorithm for the other group M subtypes was developed followed by the interpretation of HIV-1 group O and HIV-2 mutations. The process of improvement is ongoing, due to the better understanding and interpretation of single and cluster mutations and the availability of new antiretroviral substances. The knowledge gained from the experience of HIV drug resistance testing has been used to establish the interpretation of HBV polymerase mutations and will be extended for the treatment of HCV infected with protease inhibitors. Copyright © 2012 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

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No abstract available [ABSTRACT FROM AUTHOR]

No abstract available Copyright © 2010 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]