Homology Test between the Nucleic Acid of an RNA Virus and the DNA in the Host Cell

Science ◽  
1962 ◽  
Vol 138 (3546) ◽  
pp. 1270-1272 ◽  
Author(s):  
R. H. Doi ◽  
S. Spiegelman
Keyword(s):  
2020 ◽  
Vol 11 ◽  
Author(s):  
Puneet Kaur Randhawa ◽  
Kaylyn Scanlon ◽  
Jay Rappaport ◽  
Manish K. Gupta

Recently, we have witnessed an unprecedented increase in the number of patients suffering from respiratory tract illness caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The COVID-19 virus is a single-stranded positive-sense RNA virus with a genome size of ~29.9 kb. It is believed that the viral spike (S) protein attaches to angiotensin converting enzyme 2 cell surface receptors and, eventually, the virus gains access into the host cell with the help of intracellular/extracellular proteases or by the endosomal pathway. Once, the virus enters the host cell, it can either be degraded via autophagy or evade autophagic degradation and replicate using the virus encoded RNA dependent RNA polymerase. The virus is highly contagious and can impair the respiratory system of the host causing dyspnea, cough, fever, and tightness in the chest. This disease is also characterized by an abrupt upsurge in the levels of proinflammatory/inflammatory cytokines and chemotactic factors in a process known as cytokine storm. Certain reports have suggested that COVID-19 infection can aggravate cardiovascular complications, in fact, the individuals with underlying co-morbidities are more prone to the disease. In this review, we shall discuss the pathogenesis, clinical manifestations, potential drug candidates, the interaction between virus and autophagy, and the role of coronavirus in exaggerating cardiovascular complications.


1971 ◽  
Vol 232 (31) ◽  
pp. 143-145 ◽  
Author(s):  
WERNER E. G. MÜLLER ◽  
RUDOLF K. ZAHN ◽  
HANS J. SEIDEL

2021 ◽  
Vol 102 (12) ◽  
Author(s):  
Li Zhu ◽  
Xinyu Li ◽  
Henan Xu ◽  
Lifeng Fu ◽  
George Fu Gao ◽  
...  

The matrix protein of many enveloped RNA viruses regulates multiple stages of viral life cycle and has the characteristics of nucleocytoplasmic shuttling. We have previously demonstrated that matrix protein 1 (M1) of an RNA virus, influenza virus, blocks host cell cycle progression by interacting with SLD5, a member of the GINS complex, which is required for normal cell cycle progression. In this study, we found that M protein of several other RNA viruses, including VSV, SeV and HIV, interacted with SLD5. Furthermore, VSV/SeV infection and M protein of VSV/SeV/HIV induced cell cycle arrest at G0/G1 phase. Importantly, overexpression of SLD5 partially rescued the cell cycle arrest by VSV/SeV infection and VSV M protein. In addition, SLD5 suppressed VSV replication in vitro and in vivo, and enhanced type Ⅰ interferon signalling. Taken together, our results suggest that targeting SLD5 by M protein might be a common strategy used by multiple enveloped RNA viruses to block host cell cycle. Our findings provide new mechanistic insights for virus to manipulate cell cycle progression by hijacking host replication factor SLD5 during infection.


1992 ◽  
Vol 14 (5) ◽  
pp. 773-782 ◽  
Author(s):  
Etsuro Kuramoto ◽  
Norimitsu Watanabe ◽  
Daiji Iwata ◽  
Osamu Yano ◽  
Shizuo Shimada ◽  
...  

1955 ◽  
Vol 53 (4) ◽  
pp. 474-486 ◽  
Author(s):  
L. Hoyle ◽  
W. Frisch-Niggemeyer

SummaryInfluenza A virus labelled with radiophosphorus was introduced as a primary inoculum into the allantoic sac of fertile eggs. Virus so introduced enters the cells of the chorio-allantoic membrane, and a study has been made of the chemical state of 32P present in the membranes 1½ hr. after inoculation.It was found that on entry into the host cell the virus particle disintegrates probably as a result of destruction of its phospholipid. Radiophosphorus derived from the virus phospholipid can be recovered from the infected membranes by extraction with physiological saline in the form of compounds of small molecular weight which are not precipitated by protein precipitants and are not sedimentable at a centrifugal force of 100,000 g.Saline extracts of the infected membranes also contain labelled nucleic acid which appears to be derived from the virus nucleoprotein.A large part of the nucleoprotein phosphorus of the inoculated labelled virus cannot be recovered from the infected membranes by extraction with physiological saline but can be recovered if the cell nuclear material is dissolved in molar sodium chloride. The 32P in such molar chloride extracts is partly precipitated with the deoxyribonucleoprotein on dilution with water, and is partly present as free nucleic acid.It is suggested that on entry into the host cell the virus particle is broken down, the phospholipid being destroyed and the nucleoprotein disintegrated with the release of free nucleic acid which enters into a close relation with the cell nuclear material.


2021 ◽  
Author(s):  
Royce Ing ◽  
Kimberley Gilbride

CRISPR (Clustered Regularly Interspaced Small Palindromic Repeats) and Cas (CRISPR associated) proteins comprise an adaptive immune system in prokaryotes CRISPR Cas systems digest invading nucleic acids and incorporate a 30 bp snippet (“spacer") of the invader into the host genome Spacers are transcribed into CRISPR RNAs (crRNA's) that recognize the same nucleic acid in the event of a repeat invasion and guide nucleases to the target for elimination We hypothesize that a plasmid vector, when transformed into a host cell, could exogenously express a CRISPR/Cas system and prevent the host’s participation in conjugative processes


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