ABSTRACT
The COVID-19 pandemic due to SARS-CoV-2 has proven to be a tremendous challenge to the medical community. The greatest challenge since the turn of the century. The authors summarized the main cardiovascular (CV) complications and mechanisms of COVID-19 and its vaccines. COVID-19 has lung tropism, but it has been reported to affect the CV system as well. The presence of comorbidities such as hypertension, CV disease, diabetes, and chronic obstructive pulmonary disease increased the risk of developing serious complications and in turn mortality significantly. The common CV complications include cardiac arrhythmia, myocardial infarction, myocarditis, and cardiac failure, which occurred in around 20% of all COVID-19 patients. The present difficulty in the diagnosis of CV complications were that COVID-19 symptoms often mimic CV events. Furthermore, the rapid diagnosis and management of serious CV events are sometimes overlooked due to COVID-19. Access to medical treatments were sometimes restricted due to the limited healthcare resources during the pandemic. The advent of various covid vaccines have reduced the number of these complications. However, CV events following mRNA vaccines or adenoviral vector vaccines are recognized as well as myocarditis and vaccine-induced immune thrombotic thrombocytopenia. With increasing experience in managing covid patients with CV complications, physicians are becoming better equipped in preventing, detecting, and treating these complications.
ABSTRACT
Corona virus disease 2019 (COVID-19) is an emerging pandemic of highly contagious caused by severe acute respiratory syndrome coronavirus -2 (SARS-CoV-2). Understanding the infectivity of various clinical samples and its transmission routes have been the main focus of current researches since the causative pathogens was identified. In this comprehensive review, we discuss the viral shedding from different clinical samples and reveal that infectious virus may be mainly discharged through respiratory and digestive systems. Also, SARS-CoV-2 showed a potential tropism for eyes, kidney, testis, placenta and other extrapulmonary tissues and high viral loads correlated with severe conditions. A better understanding of viral shedding may help the studies on pathogenesis and transmission of SARS-CoV-2 and provide suggestions for the disease control.
ABSTRACT
Emergence of avian infectious bronchitis virus (IBV) variants with altered tissue tropism and host range has been reported from different parts of the world. Little is known about the different IBV variants existing and emerging in India. To explore the same, an IBV isolate, namely B17 isolated from backyard chicken in Tamil Nadu was used in the present study. The complete genome of B17 was sequenced and its phylogenetic relationship with the existing vaccine strain genotypes was analysed. The phylogenetic analysis of both S1 gene and complete genome sequence grouped B17 under Mass41 genotype comprising of M41, Beaudette, H120 and H120 variant with bootstrap value of 95-100%. Further, genomic analysis of B17 revealed the possibilities of emergence of the same from H120 vaccine strain through mutations at various genes.
ABSTRACT
Human coronaviruses (CoVs) can cause respiratory infection epidemics that sometimes expand into globally relevant pandemics. All human CoVs have sister strains isolated from animal hosts and seem to have an animal origin, yet the process of host jumping is largely unknown. RNA interference (RNAi) is an ancient mechanism in many eukaryotes to defend against viral infections through the hybridization of host endogenous small RNAs (miRNAs) with target sites in invading RNAs. Here, we developed a method to identify potential RNAi-sensitive sites in the viral genome and discovered that human-adapted coronavirus strains had deleted some of their sites targeted by miRNAs in human lungs when compared to their close zoonic relatives. We further confirmed using a phylogenetic analysis that the loss of RNAi-sensitive target sites could be a major driver of the host-jumping process, and adaptive mutations that lead to the loss-of-target might be as simple as point mutation. Up-to-date genomic data of severe acute respiratory syndrome coronavirus 2 and Middle-East respiratory syndromes-CoV strains demonstrate that the stress from host miRNA milieus sustained even after their epidemics in humans. Thus, this study illustrates a new mechanism about coronavirus to explain its host-jumping process and provides a novel avenue for pathogenesis research, epidemiological modeling, and development of drugs and vaccines against coronavirus, taking into consideration these findings.