14 Structure and Genome of Viruses & Viral Infection Notes 2024

Nucleocapsid = capsid coat plus enclosed nucleic acid; it is the basic viral particle containing the genome and capsid proteins.

Mostly 20–300 nm in diameter (some giant viruses up to ~500 nm).

Capsid shapes include rod-shaped, polyhedral, or more complex structures.

Enveloped viruses have a lipid membrane derived from the host; naked viruses lack this envelope.

Viruses are non-cellular obligate intracellular parasites composed of nucleic acids (DNA or RNA) enclosed in a protein capsid; some have a lipid envelope with glycoprotein spikes.

Protects nucleic acid, aids attachment to host cell receptors, enables penetration or injection of genome, may contain viral enzymes.

Protein subunits that make up the capsid coat.

DNA or RNA; genomes can be linear or circular, single- or double-stranded, exist as single molecules or multiple segments/copies.

Composed of phospholipids and cholesterol derived from host membrane during budding; contains viral glycoprotein spikes used for attachment.

They are non-cellular and don’t fit the definition of living cells yet can display life-like properties inside hosts; they don’t grow by cell division.

Attachment/adsorption; penetration/entry; replication; assembly and maturation; exit/release.

By lysis of the host cell.

By budding from the host cell membrane.

Viruses that infect bacteria and reproduce inside them using bacterial machinery.

Capsid head with linear double-stranded DNA, tail with hollow tube, contractile sheath, base plate and tail fibres for attachment.

Viral reproductive cycle culminating in host cell death and release of progeny via lysis; used by virulent phages like T4.

Contractile sheath contracts, driving hollow tail tube through bacterial cell wall; DNA is injected into host, leaving empty capsid outside.

Time between infection and appearance of mature infectious phages inside the host; no infectious particles are assembled yet.

A phage-encoded lysozyme hydrolyses the peptidoglycan cell wall, causing lysis and release of phage progeny.

Phage genome integrates into host chromosome as prophage and replicates with host DNA without producing new phage particles until induction.

Adverse conditions (e.g., UV, chemicals) causing proteases to degrade repressor proteins, allowing prophage genes to be expressed and enter lytic cycle.

Enveloped RNA virus with genome of 8 separate segments of single-stranded RNA coding for proteins including haemagglutinin and neuraminidase.

Mediates attachment to target cells and entry of the viral genome.

Enzyme involved in release of newly formed influenza viruses from infected cells by cleaving sialic acid residues.

HA binds to sialic acid-containing receptors on epithelial cells in respiratory tract (mammals) or intestines (birds).

By endocytosis into an endosome; low pH triggers HA conformation change leading to fusion of viral envelope with endosomal membrane and release of nucleocapsid.

Enzymatic removal of capsid coat releasing viral RNA, accessory proteins, and RNA-dependent RNA polymerase into cytoplasm.

Viral RNA and proteins enter the nucleus; RNA-dependent RNA polymerase replicates single-stranded RNA in nucleus.

Synthesized in rough ER and glycosylated in Golgi apparatus before being transported to cell surface membrane.

New nucleocapsids are assembled in the nucleus, then transported to the cell surface where viral glycoproteins are inserted for budding.

Viruses bud from host membrane with incorporated viral glycoproteins; neuraminidase cleaves sialic acid residues to free virions stuck by HA attachment.

Influenza A virus is the most virulent.

HIV is a retrovirus and carries reverse transcriptase, which synthesizes DNA from an RNA template.

Two copies of linear single-stranded RNA packed with proteins including reverse transcriptase and integrase; enveloped with glycoproteins.

gp120 on the viral envelope binds to CD4 receptors on T-helper cells, triggering conformational changes facilitating entry.

Viral envelope fuses with host cell membrane mediated by conformational changes in gp41, releasing nucleocapsid into cytoplasm.

Reverse transcriptase synthesizes single-stranded DNA using viral RNA template, forms RNA-DNA hybrid, removes RNA, then synthesizes complementary DNA to form double-stranded DNA.

Viral DNA integrated into host genome by integrase; can remain silent and replicate with host DNA.

Activation of host T-helper cells during immune response leads to transcription of provirus producing viral mRNA.

Capsomeres synthesized by free ribosomes; glycoproteins synthesized in rough ER and glycosylated in Golgi.

Capsid assembled around RNA and enzymes in cytoplasm; glycoproteins inserted into membrane; budding releases immature virions, then HIV protease cleaves polyproteins to mature proteins.

By budding from host membrane; maturation requires HIV protease rather than neuraminidase.

Both bind specific receptors and undergo conformational changes to facilitate entry.

Influenza enters via endocytosis and fusion within endosomes; HIV fuses directly with the host cell membrane after receptor binding.

Mutations during replication due to error-prone viral enzymes and lack of proofreading; different enzymes have different error rates.

DNA polymerase: ~1 per 10^7–10^9 nt; Influenza RNA-dependent RNA polymerase: ~1 per 10^3–10^5 nt; HIV reverse transcriptase: ~1 per 1700 nt.

Gradual accumulation of mutations in viral RNA coding for glycoproteins, producing slightly modified glycoproteins and enabling reinfection.

Because small changes in glycoproteins reduce effectiveness of existing antibodies, allowing reinfection and seasonal epidemics.

Major change in virus structure from genetic reassortment between different influenza viruses, creating new subtypes with new glycoprotein combinations.

Pigs can be infected by avian, human, and swine influenza viruses and have receptors for multiple sialic acid types, enabling reassortment when co-infected.

When co-infection of one host cell by different influenza viruses leads to progeny virions containing RNA segments from multiple virus types.

High variation produces new strains that evade immunity and vaccines, making permanent worldwide elimination difficult.

By killing host cells, inhibiting host DNA/RNA/protein synthesis, depleting raw materials, and triggering immune responses that damage tissues.

Death of ciliated epithelial cells impairs mucus clearance, increasing susceptibility to other infections and causing symptoms like fever, sore throat, cough, and possibly pneumonia.

Children <2 years, adults ≥65 years, and people with chronic lung disease or weakened immune systems.

1918 Spanish flu (H1N1, 20–100 million deaths), 1957 Asian flu (H2N2), 1968 Hong Kong flu (H3N2), 2009 H1N1 pandemic.

To treat or prevent secondary bacterial infections that occur due to impaired mucociliary clearance after influenza damages epithelial cells.

They recognize antigen presented on MHC II via CD4, become activated, release cytokines, and stimulate macrophages, killer T cells, and B cells to produce antibodies.

By targeting and killing T-helper cells (via gp120-CD4 binding), impairing immune function and allowing opportunistic infections and cancers.

Fusion of infected T-helper cells with neighbouring cells due to gp120/gp41 expressed on cell membrane, forming multinucleated giant cells and enhancing cell death.

Insertion of viral DNA near proto-oncogenes or disruption of tumor suppressor genes can lead to overexpression or activation, promoting oncogenesis.

HIV can persist in latent proviral form integrated into host DNA; high mutation rate and latency prevent eradication and complicate vaccine development.

Antiretroviral drugs inhibit reverse transcriptase, HIV protease, and other viral enzymes to suppress replication; therapy is typically lifelong.

Often a latency period of ~8–10 years before AIDS symptoms manifest.