Immune Responses to Viral Infections & Influenza

30 question-and-answer flashcards covering viral entry, influenza structure and classification, innate and adaptive immune responses to viruses, antibody functions, viral survival and immune-evasion tactics, and influenza antigenic variation.

Which two surface glycoproteins of influenza A facilitate (a) attachment to host cells and (b) release of progeny virions?

(a) Hemagglutinin (HA) binds sialic-acid residues for attachment; (b) Neuraminidase (NA) cleaves sialic acid to allow budding and release.

What type of genome does the influenza virus possess?

An enveloped, segmented, single-stranded negative-sense RNA genome (8 segments).

How many RNA segments and total proteins are encoded by influenza A virus?

Eight ssRNA segments encoding approximately ten proteins.

List four common routes by which viruses enter the body.

Across mucosa of the respiratory tract, gastrointestinal tract, genitourinary tract, through broken skin, or via arthropod/animal bites.

What two molecular interactions are required for influenza to enter a host cell?

1) HA binding to sialic-acid adhesion molecules; 2) interaction with entry receptors such as clathrin-mediated endocytosis.

On what viral proteins is influenza A, B, and C typing based?

The nucleoprotein (NP) and matrix (M1) proteins.

Which influenza type is responsible for most pandemics?

Influenza Type A.

How many haemagglutinin (HA) and neuraminidase (NA) subtypes are recognised in influenza A?

13 HA subtypes and 9 NA subtypes.

Give one example each of a swine-origin and an avian-origin influenza A subtype.

Swine origin: H1N1; Avian origin: H5N1.

What are the roles of influenza M1 and M2 proteins?

M1 is the main capsid protein; M2 is an ion channel crucial for uncoating the viral genome.

During a first encounter with a virus, which antibody class appears quickly without prior antigen exposure?

Natural (germline) IgM.

State two protective functions of natural IgM antibodies.

They neutralise or lyse viruses via complement activation and enhance phagocytic clearance of apoptotic or infected cells.

Which two cytotoxic cell types limit viral spread before adaptive immunity develops?

Natural Killer (NK) cells and cytotoxic T (Tc/CD8+) lymphocytes.

Which cytokines are produced by virus-infected non-immune cells and what are their main antiviral effects?

Type I interferons (IFN-α/β) and IL-12; they inhibit viral protein synthesis, induce RNA degradation (RNase L), and activate NK cells.

How do type I IFNs and IL-12 promote early killing of infected cells?

They stimulate NK cells, which induce apoptosis of the infected cells.

What is antigen ‘cross-presentation’ by dendritic cells?

Uptake of exogenous viral antigens and their presentation on MHC class I molecules to activate naïve CD8+ T cells.

Following influenza infection, how long do anti-HA antibody titres typically remain stable and why?

They peak after a few days, decline over six months, but memory B cells maintain stability for years.

List four mechanisms by which antibodies neutralise or eliminate viruses.

1) Block attachment to cellular receptors; 2) neutralise fusion/post-binding events; 3) inhibit release of progeny virus; 4) mediate ADCC by NK cells.

How can antibodies plus complement combat enveloped viruses specifically?

By activating the classical complement pathway, leading to membrane attack complex-mediated lysis of the virion envelope.

State three early non-specific host defences against viral replication.

Fever, type I interferon production, and NK-cell cytotoxicity.

Name four general survival strategies that enable viruses to persist in host populations.

Long latency (e.g., HIV), rapid transmission during acute illness (influenza), infection of multiple species (West Nile), and immune evasion mechanisms.

How do some herpesviruses subvert phagocytes?

They express surface proteins that inhibit macrophage activation, reducing phagocytosis.

Give one example of viral manipulation of the complement system.

HCMV induces host complement-inhibitory proteins to protect infected cells; HSV-1 encodes its own complement inhibitors.

How does hepatitis C virus block the antiviral action of interferons?

By inhibiting PKR activity, thereby allowing viral protein synthesis to continue.

What is the mechanism by which HSV impairs antigen presentation via MHC I?

HSV expresses ICP47, which inhibits the TAP transporter, preventing peptide loading onto MHC I.

Which viruses down-regulate (a) MHC I and (b) MHC II expression on host cells?

(a) Adenoviruses and cytomegalovirus (CMV) down-regulate MHC I; (b) HIV, measles virus, and CMV down-regulate MHC II.

How do certain herpesviruses neutralise antibodies already bound to them?

They bind the Fc region of IgG, preventing interaction with Fc receptors and complement.

Define ‘antigenic drift’ in influenza viruses.

Gradual accumulation of spontaneous point mutations causing minor changes in HA and NA, producing new seasonal strains.

Define ‘antigenic shift’ in influenza viruses.

Sudden appearance of a novel HA and/or NA subtype via genetic reassortment, creating a virus markedly different from previous strains.

Why are antigenic shifts more likely than drifts to cause pandemics?

Because the new HA/NA combinations are unfamiliar to human immune systems, resulting in little or no pre-existing immunity.