MICB 212 Final Exam Prep (Virology) Cartes | Quizlet

What is a virus?

An independent nucleic acid genome (DNA or RNA, never both) that replicates inside a host cell by hijacking the host's biosynthetic machinery; obligate intracellular parasite.

What is the basic structure of viruses?

Genome (DNA or RNA; ss or ds; sometimes segmented) + protein coat (capsid built from capsomeres) + lipid envelope (acquired from host membrane).

What are the types of capsid symmetry in viruses?

Helical, icosahedral, or complex.

What is the central dogma of molecular biology?

DNA → (transcription) → mRNA → (translation) → protein.

How do RNA viruses deviate from the central dogma?

Some RNA viruses replicate RNA→RNA, and retroviruses use reverse transcription (RNA→DNA→RNA).

+ RNA vs - RNA: What is the difference?

(+) RNA: same polarity as mRNA, can be translated directly. (-) RNA: complementary to mRNA; must be copied into (+) RNA before translation.

What is a polyprotein?

A single long polypeptide translated from one open reading frame (ORF) that is cleaved into functional viral proteins.

What does it mean for a cell to be susceptible to a virus?

The cell expresses receptor(s) permitting virus entry.

What does it mean for a cell to be permissive to a virus?

The cell provides intracellular machinery to permit replication.

What are the key steps of a virus replication cycle?

Attachment, entry, replication and expression, assembly, egress.

What happens during the attachment phase of a virus replication cycle?

Reversible collisions followed by specific binding to receptors on the host cell.

How does a virus enter a host cell?

Through receptor-mediated endocytosis or membrane fusion.

What is the role of viral polymerase in replication?

It may be required for genome replication and synthesis of viral mRNAs and proteins.

What is the Baltimore classification system?

It groups viruses by genome type and how mRNA is produced.

What are the possible outcomes of a virus infection in a eukaryotic cell?

Lytic/acute, persistent/chronic, latent, oncogenic.

What is the IPV vaccine?

Inactivated poliovirus vaccine (Salk): injected, formalin-inactivated virus.

What are the advantages of IPV?

Safe for immunodeficient people, induces serum IgG (systemic protection).

What are the disadvantages of IPV?

Does not induce mucosal IgA, requires boosters, administration logistics.

What is the OPV vaccine?

Oral poliovirus vaccine (Sabin): live attenuated, oral.

What are the advantages of OPV?

Induces mucosal IgA and systemic immunity, easy to deliver, rapid protection.

What are the disadvantages of OPV?

Rare reversion to neurovirulent form, not safe for immunodeficient individuals.

Describe the structure of the poliovirus capsid.

Non-enveloped, ~30nm, icosahedral capsid of 60 promoters.

What is the genome of poliovirus?

Single stranded (+) RNA, 5' linked VPg protein, long 5' UTR with IRES, 3' poly (A) tail.

How does poliovirus enter the host cell?

Binds CD155 (PVR) on epithelial cells, monocytes/macrophages, and CNS neurons.

How does poliovirus eliminate competition for translation?

It encodes a protease that cleaves host translation factor eIF4G, shutting off cap-dependent host mRNA translation.

How does poliovirus replicate its genome?

Using RNA-dependent RNA polymerase (RDRP) to synthesize (-) strand from the (+) template.

How are poliovirus progeny assembled and released?

Capsid proteins self-assemble into procapsids, packaging selects (+) RNA, maturation cleavage yields infectious particles.

What is the structure of the influenza virus particle?

Enveloped, pleomorphic (80-120 nm), with surface spikes: hemagglutinin (H) and neuraminidase (N); internal M1 (matrix) and M2 (ion channel); RNPs (RNA + NP + polymerase complex).

How is the influenza virus genome organized?

Segmented (8 pieces) single-stranded (-) RNA; each segment packaged with NP and a polymerase complex (PB1, PB2, PA). Some segments encode more than one protein via splicing/alternative reading.

What is the nomenclature for naming influenza viruses?

Type / location / strain number / year / subtype (e.g., A/Perth/16/2019 (H3N2)). Influenza A subtypes are defined by H and N combinations H1-H18, N1-N11.

What is the host range of influenza A viruses?

Infects humans, birds, pigs, and other mammals; wild aquatic birds are the reservoir, and pigs are important intermediate hosts.

What is the function of hemagglutinin (H) in influenza viruses?

Hemagglutinin (H) binds sialic acid on host glycoproteins, mediating attachment and membrane fusion after proteolytic activation.

What is the role of neuraminidase (N) in influenza viruses?

Neuraminidase (N) cleaves sialic acid residues to release newly budded virions and prevent self-aggregation/reinfection of the same cell.

What modifications are needed for hemagglutinin to release the virus genome into the cell?

Proteolytic cleavage of precursor H0 into HA1 and HA2 exposes the fusion peptide; low pH-triggered conformational change inside the acidified endosome exposes the fusion peptide and drives fusion with the endosomal membrane.

Why must the influenza virus package its own RNA-dependent RNA polymerase (RDRP)?

The (-) RNA genome cannot be transcribed by host RNA polymerase II; influenza packages its own RDRP (PB1/PB2/PA) to transcribe (-)RNA to (+)mRNA.

How does the influenza virus steal the 5'-methylated cap from cellular mRNA?

PB2 binds to the 5' methylated cap from host pre-mRNAs, and PA cleaves downstream; the short capped oligo is used as a primer to synthesize viral mRNA.

How does the full-length anti-genomic RNA differ from mRNA?

Both are (+) polarity; mRNAs are capped and polyadenylated short transcripts for translation, while the antigenome/full-length +RNA is the full-length complement used as a template for genome replication.

Describe the replication of the influenza virus genome.

RNPs are replicated in the nucleus; RNPs + M1/M2 and glycoproteins assemble at the plasma membrane, the virus buds, and N cleaves sialic acid to free the virion.

What is the role of neuraminidase in the release of the virus particle?

Neuraminidase cleaves sialic acid to free the virion.

What disease is caused by the influenza virus?

Acute respiratory infection (upper and lower tract), with symptoms driven by virus replication and host immune response; complications include pneumonia and secondary bacterial infections.

How do anti-viral medications interfere with virus progeny production?

Drugs can target viral entry/uncoating (M2 inhibitors), neuraminidase to block release, or polymerase function, reducing progeny production.

What is antigenic drift and shift in influenza viruses?

Drift is the gradual accumulation of point mutations in H/N leading to seasonal epidemics; shift is the reassortment of genome segments when two different strains co-infect the same cell, leading to sudden major changes.

Why are pigs important in the formation of new influenza strains?

Pigs can be infected by both avian and human influenza strains, enabling reassortment and generation of novel A strains with pandemic potential.

What types of vaccines are available for influenza prevention?

Seasonal vaccines are updated annually to match circulating strains due to continuous antigenic drift; immunity wanes, necessitating repeated immunization.

How does HIV bind to susceptible cells?

Gp120 binds CD4 on helper T cells, macrophages, and dendritic cells, causing a conformational change that recruits a co-receptor (CCR5 or CXCR4) and exposes the fusion peptide.

What is the process of reverse transcription in HIV?

Virus packages reverse transcriptase (RT) that converts ss RNA to ds DNA within the reverse transcription complex; tRNA serves as a primer for first strand synthesis.

How does HIV integrate its genome after reverse transcription?

Integrase catalyzes the insertion of proviral dsDNA into host chromosomal DNA, establishing permanent infection.

What is required for genome expression in HIV?

Host RNA pol II transcribes the integrated provirus to produce mRNA and genomic RNA; frameshifting and RNA splicing are necessary for producing the correct viral proteins.

Describe the process of virus assembly and maturation in HIV.

Gag directs particle assembly at the plasma membrane; budding uses host ESCRT machinery, and viral protease cleaves Gag/Gag-pol into mature components.

What is the pathogenesis of AIDS?

Progressive loss of CD4 T cells leads to immunodeficiency, opportunistic infections, certain cancers, and eventual AIDS when immune function fails.

What are the clinical stages of HIV infection?

Incubation, acute infection, latency, and AIDS diagnosis.

How can the spread of HIV be controlled and prevented?

Reduce exposure to infected fluids through safe sex, blood screening, needle programs, prevention of vertical transmission, and education.

What is the role of antiretroviral therapy (ART) in HIV?

ART reduces viral load to undetectable levels and prevents transmission.

How do reverse transcriptase inhibitors work?

They block RT activity, preventing the conversion of RNA to proviral DNA, thus not establishing permanent infection.

How do protease inhibitors prevent HIV replication?

They inhibit viral protease, preventing the cleavage of Gag/Gag-pol, resulting in immature and non-infectious viral particles.

What are the challenges in producing and testing a new HIV vaccine?

Natural infection does not provide sterilizing immunity, lack of perfect animal models, safety concerns, high viral diversity, and ethical constraints on human testing.

What is the strategy of the influenza virus for mRNA production?

Influenza is a segmented (-)mRNA virus that performs cap-snatching and makes monocistronic mRNAs from separate genome segments.

How does rabies virus produce mRNA?

Rabies is a non-segmented (-) RNA virus that synthesizes a 5' cap, adds poly-A tails, and generates monocistronic mRNAs through sequential transcription.

What is the assembly process of the rabies virus?

Glycoprotein G is synthesized in the ER, transported to the plasma membrane, and connects with the NP-coated genome to form the nucleocapsid.

How does rabies virus egress from the cell?

Rabies buds through the plasma membrane, capturing a membrane patch to form the enveloped virus particle.

What are potential targets for antiviral therapy against rabies?

L polymerase, M protein, G glycoprotein, and P protein.

What is the primary vaccine target for rabies?

The G glycoprotein, responsible for attachment and inducing neutralizing antibodies.

How does an RNA vaccine induce B cell immunity?

It delivers mRNA encoding a pathogen antigen, which is taken up by host cells, leading to antigen synthesis and B cell activation.

What are the safety advantages of RNA vaccines?

RNA is non-infectious and non-integrating, posing no risk of disease or insertion into the host genome.

What are the manufacturing advantages of RNA vaccines?

Rapid production and no need for eggs or cell-culture systems, making it scalable and cost-effective.

What are the four types of vaccines for COVID-19?

mRNA, viral vector, inactivated viruses, and subunit vaccines.

How do mRNA vaccines work?

They deliver nucleoside-modified mRNA encoding the SARS-CoV-2 spike protein, which is synthesized by host cells.

What are the storage requirements for mRNA vaccines?

Moderna requires -20℃ and Pfizer requires -70℃ for stability.

What are the pros and cons of viral vector vaccines?

Pros: more stable at refrigerator temperature; Cons: slower to modify and pre-existing immunity can reduce efficacy.

What are the advantages of inactivated virus vaccines?

Classic technology, well understood, and does not require freezing.

What are the disadvantages of subunit vaccines?

Requires adjuvants and slower protein production compared to mRNA vaccines.