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Revisione. Introduction C-reactive protein (CRP) is the key biomarker for diagnosing and monitoring inflammatory conditions. However, challenges arise when patients exhibit elevated CRP levels without an evident inflammatory cause. Despite the performance of CRP assays using immunoturbidimetry, this method remains sensitive to interferences that may result in false positive results. Case reports Drawing from three case studies illustrating analytical interferences in CRP measurements, we propose a comprehensive review of the literature on this subject. The most common cause of analytical interference in CRP measurement is the binding of rheumatoid factor to capture antibodies, generating a signal detected by immunoturbidimetry despite the absence of CRP in the sample. To identify such interferences, various antibody neutralization techniques and alternative assay methods can be employed. Reporting falsely elevated CRP levels may lead to

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Revisione. Several bat species asymptomatically harbor certain viruses that are highly pathogenic in other mammals. The underlying mechanisms involve an evolutionary balance between tolerance and immune resistance to viral infections. However, how bats innate immunity has evolved in response to viruses remains to be elucidated. Here, we review the evolution of the protein kinase R (PKR) in bats, a major antiviral protein of vertebrate innate antiviral defense. Our recent results indicate that PKR has evolved under selective pressure and has undergone genomic duplications in bats, in contrast to all mammals studied, which possess only a single copy of the gene. The genetic changes in bat PKR are probably partly the result of genetic conflicts with ancient pathogenic poxviruses, shaping a bat-specific host–virus interface. Furthermore, the duplicated PKRs in Myotis species enable them to collectively escape viruses and enhance their viral

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Revisione. Thrombotic Thrombocytopenic Purpura (TTP) is a rare disease characterized by a severe deficiency of ADAMTS13, the specific protease that cleaves von Willebrand factor. The congenital form of TTP (cTTP) results from pathogenic variants of the ADAMTS13 gene. cTTP has two peaks of incidence: one in childhood and the other in adulthood, mainly in an obstetric context. The treatment of cTTP relies on ADAMTS13 replacement therapy for prophylaxis or on-demand, depending on the evolving nature of the disease, along with the management of cardiovascular risk factors. The historical treatment for cTTP has been substitution plasma therapy. Since 2017, a recombinant human ADAMTS13 protein (rhADAMTS13) has been evaluated in cTTP in international clinical trials. The rhADAMTS13 protein, intravenous infusion used for prophylaxis or on-demand, has been granted early access or compassionate use in cTTP in France in 2024. The objective of this

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Revisione. Orthoflaviviruses are enveloped positive-sense RNA viruses comprising numerous human pathogens transmitted by hematophagous arthropods. This includes viruses such as dengue virus, Zika virus, and yellow fever virus. The viral nonstructural protein NS1 plays a central role in the pathogenesis and cycle of these viruses by acting in two different forms: associated with the plasma membrane (NS1m) or secreted outside the cell (NS1s). The versatility of NS1 is evident in its ability to modulate various aspects of the infectious process, from immune evasion to pathogenesis. As an intracellular protein, it disrupts many processes, interfering with signaling pathways and facilitating viral replication in concert with other viral proteins. As a secreted protein, NS1 actively participates in immune evasion, interfering with the host immune system, inhibiting the complement system, facilitating viral dissemination, and disrupting the in

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Pubblicazione 2021 — abstract non disponibile: non vengono dedotti risultati.

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Pubblicazione 2020 — abstract non disponibile: non vengono dedotti risultati.

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