Human Anatomy & Physiology (11th Edition)
11th Edition
ISBN: 9780134580999
Author: Elaine N. Marieb, Katja N. Hoehn
Publisher: PEARSON
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Question
If HIV was just an enveloped virus, but not a retrovirus, which of the following drugs would likely still work?
NtRTI
NRTI
Integrase inhibitor
Entry inhibitor
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- Knowing that retroviruses operate on the principle of reversing thedirection of transcription from RNA to DNA, propose a drug thatmight possibly interfere with their replication.arrow_forwardWhich of the following statements are correct for a class V ssRNA (-) virus? it uses its genome directly for translation it must make the complementary (+) RNA strand to synthesize more of its genome it replicates its genome via classical semiconservative replication it converts its genome to DNA via reverse transcriptase as part of its life cyclearrow_forwardReverse transcriptase would most likely be inside which virus? a DNA-based lytic virus an RNA-based lysogenic virus an RNA-based lytic virus a DNA-based lysogenic virusarrow_forward
- Which step(s) in the replication cycle of HIV can still occur in the presence of a reverse transcriptase inhibitor? Select all that apply. transcription of viral genes initial viral attachment viral assembly integration of viral DNA into host genome initial viral entryarrow_forwardHow do some bacteria protect themselves against the viruses? protect themselves by making antibodies mutating the virus genome revers transcriptase assemble the capsid restriction enzymearrow_forwardWhat is the purpose of reverse transcriptase in retroviruses? It translates viral RNA into proteins. It converts host cell RNA into viral DNA. It uses viral RNA as a template for DNA synthesis. It uses viral RNA as a template for making more viral RNA strands.arrow_forward
- Tat and Rev proteins are required for HIV replication. What are their roles and why are they essential to the virus?arrow_forwardanswer doesn't have to be long i just need an explanation, thank you! The whole world right now is concerned (or they should be) about the appearance of new variants of SARS-CoV-2. Among other things, these variant viruses have mutations that change the amino acid sequence of the spike protein on the virus surface. While this is concerning, I would like to propose that there is a limit to how far these mutations can change the spike protein. Why can't there be an endless number of new mutations of this viral protein? How would these amino acid changes affect how the virus works?arrow_forward
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