ABSTRACT
Viral infections have been linked to a variety of cardiac pathology, which may include acute myocarditis, dilated cardiomyopathy, heart failure, cardiogenic shock, pericarditis, acute coronary syndromes, and arrhythmias. We performed a systematic review of literature focusing on the cardiovascular effects of various viral infections, as well as providing an update on the current understanding of the pathophysiology of Coronavirus disease-2019 (COVID-19). Cardiac manifestations of viral illnesses are usually self-limiting, have variable clinical presentations, and require sufficient clinical suspicion for diagnosis and optimal management.
ABSTRACT
We describe 3 adult patients who did not have COVID-19 but instead had a treatable tick-borne infection. In each case, however, the duration of time until diagnosis was delayed due to issues that have arisen because of the COVID-19 pandemic. These issues need to be addressed to preserve patient well-being.
Subject(s)
COVID-19/epidemiology , Pandemics , Tick-Borne Diseases/diagnosis , Adult , Aged , Delayed Diagnosis , Female , Humans , Male , Middle Aged , SARS-CoV-2 , Tick-Borne Diseases/etiology , Tick-Borne Diseases/therapyABSTRACT
Flaviviruses pose a constant threat to human health. These RNA viruses are transmitted by the bite of infected mosquitoes and ticks and regularly cause outbreaks. To identify host factors required for flavivirus infection, we performed full-genome loss of function CRISPR-Cas9 screens. Based on these results, we focused our efforts on characterizing the roles that TMEM41B and VMP1 play in the virus replication cycle. Our mechanistic studies on TMEM41B revealed that all members of the Flaviviridae family that we tested require TMEM41B. We tested 12 additional virus families and found that SARS-CoV-2 of the Coronaviridae also required TMEM41B for infection. Remarkably, single nucleotide polymorphisms present at nearly 20% in East Asian populations reduce flavivirus infection. Based on our mechanistic studies, we propose that TMEM41B is recruited to flavivirus RNA replication complexes to facilitate membrane curvature, which creates a protected environment for viral genome replication.