Coronavirus Replication and Reverse Genetics (Current Topics by Luis Enjuanes

By Luis Enjuanes

Human coronaviruses brought on the SARS epidemic that contaminated greater than 8000 humans, killing approximately ten percentage of them in 32 nations. This e-book presents crucial info on those viruses and the advance of vaccines to manage coronavirus infections.

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Additional info for Coronavirus Replication and Reverse Genetics (Current Topics in Microbiology and Immunology)

Example text

G. L. Sawicki mRNAs of coronaviruses (Baric et al. 1983). They suggested that the viral polymerase (RdRp) initiated plus strand synthesis at the 30 end of genome-length templates. In this model, after it produced the leader RNA and the IGS, the RdRp would jump from the 30 end of the minus strand all the way to one of the internal complementary copies of the IGS and reinitiate RNA synthesis. The IGS served to redirect the RdRp to an internal site and then served as a primer for elongation. This “leaderprimed transcription model” was based on three experimental findings.

Sawicki DL, Wang T, Sawicki SG (2001) The RNA structures engaged in replication and transcription of the A59 strain of mouse hepatitis virus. J Gen Virol 82:385– 396 Schaad MC, Baric RS (1994) Genetics of mouse hepatitis virus transcription: evidence that subgenomic negative strands are functional templates. J Virol 68:8169–8179 Schochetman G, Stevens RH, Simpson RW (1977) Presence of infectious polyadenylated RNA in the coronavirus avian bronchitis virus. Virology 77:772–782 Senanayake SD, Brian DA (1999) Translation from the 50 UTR of mRNA 1 is repressed, but that from the 50 UTR of mRNA 7 is stimulated in coronavirus-infected cells.

Increased exposure of the gels to compensate for this imbalance verified the presence at each time period of the subgenomic RI population. Moreover, the relative proportion of each of the seven size classes of RI was maintained at all times studied, both early and late. We interpreted our results to indicate that both genome and subgenomic minus strands are produced at the earliest times in infection and thus must be derived from input genome plus strands. We have failed so far to detect a time early in infection when only genomic minus strands are made.

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