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Abstract
Viruses can generate molecular mimicry phenomena within their hosts. Why should severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) not be considered one of these? Information in this short review suggests that it might be so and, thus, encourages research aiming at testing this possibility. We propose, as a working hypothesis, that the virus induces antibodies and that some of them crossreact with host’s antigens, thus eliciting autoimmune phenomena with devasting consequences in various tissues and organs. If confirmed, by in vitro and in vivo tests, this could drive researchers to find effective treatments against the virus.
Highlights
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) induced disease (COVID-19) is a planetary emergency that is urging many research groups to redirect their efforts and to channel their experience towards understanding its pathogenesis
The paucity of data on pathogenesis is due to a considerable extent to the very low number of autopsies that have been performed on COVID-19 victims [1]
The emerging picture is that of widespread microvascular damage, diffuse thrombosis, disseminated intravascular coagulation (DIC) and, lastly, a multiorgan failure (MOF), often leading to death (Figure 3)
Summary
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) induced disease (COVID-19) is a planetary emergency that is urging many research groups to redirect their efforts and to channel their experience towards understanding its pathogenesis. While histopathological and other data from laboratory tests and autopsies will accumulate as the pandemic persists in the few months or so, some progress can be achieved applying bioinformatics and scientific reasoning In this brief hypothesis paper, we have organized pertinent information available from the growing scientific literature and from the chats of doctors and researchers on the web that cannot be ignored at this time, they are not official instruments for dissemination of scientific data. We will focus on the disease caused when the virus invades the body via the upper respiratory tract disregarding the other ways of viral entry, which are. For unknown reasons but which are probably related to a “hyperreactivity” of both innate and acquired immunities, the disease progresses towards the third step. The emerging picture is that of widespread microvascular damage, diffuse thrombosis, disseminated intravascular coagulation (DIC) and, lastly, a multiorgan failure (MOF), often leading to death (Figure 3)
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