Translation of the poliovirus genome yields a polyprotein , a large protein with protease activity that cleaves itself into three smaller proteins. Additional cleavage activity eventually yields all the proteins needed for capsid formation, as well as an RNA-dependent RNA-polymerase.
Other possibilities include:. Minus-strand RNA viruses include many members notable for humans, such as influenza virus, rabies virus, and Ebola virus.
Upon entrance into the host cell, the plus-strand RNAs generated by the polymerase are used as mRNA for protein production. Instead, the virus uses its reverse transcriptase to synthesize a piece of ssDNA complementary to the viral genome. This allows the virus to insert its genome, in a dsDNA form, into the host chromosome, forming a provirus.
Unlike a prophage, a provirus can remain latent indefinitely or cause the expression of viral genes, leading to the production of new viruses. Excision of the provirus does not occur for gene expression. Viroids are small, circular ssRNA molecules that lack protein.
These infectious molecules are associated with a number of plant diseases. Since ssRNA is highly susceptible to enzymatic degradation, the viroid RNA has extensive complementary base pairing, causing the viroid to take on a hairpin configuration that is resistant to enzymes.
Prions are infectious agents that completely lack nucleic acid of any kind, being made entirely of protein. They are associated with a variety of diseases, primarily in animals, although a prion has been found that infects yeast! The prion protein is found in the neurons of healthy animals PrPC or Prion Protein Cellular , with a particular secondary structure. Accumulation of the pathogenic form causes destruction of brain and nervous tissue, leading to disease symptoms such as memory loss, lack of coordination, and eventually death.
Skip to content Viral Classification Since viruses lack ribosomes and thus rRNA , they cannot be classified within the Three Domain Classification scheme with cellular organisms.
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Immunization with an attenuated severe acute respiratory syndrome coronavirus deleted in E protein protects against lethal respiratory disease. Coronaviruses maintain viability despite dramatic rearrangements of the strictly conserved genome organization.
Rewiring the severe acute respiratory syndrome coronavirus SARS-CoV transcription circuit: engineering a recombination-resistant genome. A live, impaired-fidelity coronavirus vaccine protects in an aged, immunocompromised mouse model of lethal disease.
Human aminopeptidase N is a receptor for human coronavirus E. Human coronavirus NL63 employs the severe acute respiratory syndrome coronavirus receptor for cellular entry. Feline aminopeptidase N serves as a receptor for feline, canine, porcine, and human coronaviruses in serogroup I. Interspecies aminopeptidase-N chimeras reveal species-specific receptor recognition by canine coronavirus, feline infectious peritonitis virus, and transmissible gastroenteritis virus.
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The nsp2 replicase proteins of murine hepatitis virus and severe acute respiratory syndrome coronavirus are dispensable for viral replication. Severe acute respiratory syndrome coronavirus nonstructural protein 2 interacts with a host protein complex involved in mitochondrial biogenesis and intracellular signaling.
Nuclear magnetic resonance structure shows that the severe acute respiratory syndrome coronavirus-unique domain contains a macrodomain fold. Severe acute respiratory syndrome coronavirus papain-like protease ubiquitin-like domain and catalytic domain regulate antagonism of IRF3 and NF-kappaB signaling. Proteomics analysis unravels the functional repertoire of coronavirus nonstructural protein 3. Nuclear magnetic resonance structure of the N-terminal domain of nonstructural protein 3 from the severe acute respiratory syndrome coronavirus.
Nuclear magnetic resonance structure of the nucleic acid-binding domain of severe acute respiratory syndrome coronavirus nonstructural protein 3.
The autocatalytic release of a putative RNA virus transcription factor from its polyprotein precursor involves two paralogous papain-like proteases that cleave the same peptide bond. J Biol Chem.
Mutation in murine coronavirus replication protein nsp4 alters assembly of double membrane vesicles. Murine hepatitis virus nonstructural protein 4 regulates virus-induced membrane modifications and replication complex function.
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EMBO J. The severe acute respiratory syndrome-coronavirus replicative protein nsp9 is a single-stranded RNA-binding subunit unique in the RNA virus world. Molecular model of SARS coronavirus polymerase: implications for biochemical functions and drug design.
The viral genome of hepatitis C virus nonA-nonB , an elusive major infectious agent, has recently been cloned. This genome is a single positive-stranded RNA of at least 10, bases which codes for several antigens, some of them associated specifically with nonA-nonB hepatitis infections. The hepatitis D delta viral agent, an infectious agent requiring a hepadnarious for propagation, contains a covalently closed circular single-stranded RNA genome of nucleotides.
Gauss Pyramid. All Hindu Gods Wallpaper. Cell Phone Illustration. Super Lori Ball Python. People Also Search. HIV Replication Process. B-cell Life Cycle. HPV Life Cycle. Virus Life Cycle Stages. Bacteriophage Lytic Cycle. Adenovirus Life Cycle.
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