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Viral Disease Examples: Common Cold, Influenza, and HIV/AIDS (MBY161 Theme 12)

Study Guide - Smart Notes

Tailored notes based on your materials, expanded with key definitions, examples, and context.

Viral Disease Examples

Learning Outcomes

This theme covers selected examples of viral diseases relevant to microbiology, focusing on the common cold, influenza, and HIV/AIDS. Students should be able to discuss the etiology, pathogenesis, epidemiology, and treatment/prevention strategies for these diseases.

The Common Cold

Etiology and Clinical Features

  • Over 200 different viruses can cause the common cold, including rhinoviruses, coronaviruses, and others.

  • Symptoms: Sneezing, nasal secretion, congestion. May lead to laryngitis and otitis media.

  • Fever is typically absent.

  • Antibiotics are ineffective because the disease is viral, not bacterial.

  • Symptomatic relief is provided by cough suppressants and antihistamines.

  • Vaccine development is not feasible due to the large number of causative viral agents and their antigenic diversity.

Example: Rhinovirus is the most common cause, responsible for about 50% of cases.

Influenza (Flu)

Virology and Structure

  • Influenza virus (Influenzavirus) is an enveloped virus with eight RNA segments.

  • Key surface proteins: Hemagglutinin (HA) spikes (attachment) and Neuraminidase (NA) spikes (release).

  • Outer lipid bilayer and capsid layer protect the viral genome.

Clinical Features

  • Symptoms: Chills, fever, headache, muscle aches. No intestinal symptoms.

Strains and Epidemiology

  • Avian, swine, and mammalian strains exist.

  • Swine act as "mixing vessels" for new strains due to their susceptibility to both avian and human influenza viruses.

Antigenic Variation

  • Antigenic drift: Minor changes due to mutations in HA and NA genes, leading to seasonal epidemics.

  • Antigenic shift: Major changes due to genetic reassortment, often resulting in pandemics.

Prevention and Treatment

  • Mortality rate: ~1%, highest in the very young and very old.

  • Multivalent vaccines are formulated annually to target the most prevalent strains.

  • Diagnosis is difficult based on symptoms alone.

  • Antiviral drugs: Zanamivir (Relenza) and oseltamivir (Tamiflu) inhibit neuraminidase, preventing viral release.

Table: Human Influenza Viruses (Main Types)

Type

Antigenic Subtype

Host

Disease Severity

A

H1N1, H3N2, etc.

Humans, swine, birds

Severe

B

None

Humans

Moderate

C

None

Humans, swine

Mild

Additional info: Table inferred from slide and standard influenza classification.

HIV/AIDS (Human Immunodeficiency Virus / Acquired Immunodeficiency Syndrome)

History and Origin

  • 1981: First cluster of AIDS cases in the US (Pneumocystis pneumonia, Kaposi's sarcoma).

  • 1983: Discovery of HIV as the causative agent.

  • Origin: Cross-species transmission from SIV (Simian Immunodeficiency Virus) in chimpanzees to humans in Africa (~1921).

Subtypes of HIV

Subtype

Origin

Prevalence

Pathogenicity

HIV-1

Chimpanzees, gorillas

99% of cases; Group M = 90%

High

HIV-2

Monkeys, sooty mangabeys

Mostly Africa

Lower than HIV-1

Structure of HIV

  • Genus: Lentivirus (a retrovirus)

  • Genome: Two identical RNA strands

  • Enzymes: Reverse transcriptase

  • Envelope: Phospholipid with gp120 glycoprotein spikes

Pathogenicity and Infectiveness

  • Spread by dendritic cells to lymphoid organs, contacts activated T cells.

  • gp120 binds to CD4+ receptor and CCR5/CXCR4 coreceptors on T helper cells, macrophages, and dendritic cells.

  • Virus fuses and enters the cell.

  • Inside the cell, viral RNA is reverse transcribed into DNA, which integrates into host chromosomal DNA.

  • Active infection: New viruses produced.

  • Latent infection: DNA remains hidden as a provirus; some cells become memory T cells, serving as reservoirs.

  • Rapid antigenic changes and high mutation rate complicate immune response and vaccine development.

Stages of HIV Infection

  • Phase 1: Asymptomatic or lymphadenopathy.

  • Phase 2: Steady decline in CD4+ T cells; few symptoms (persistent infections, fever, oral leukoplakia).

  • Phase 3: AIDS develops; CD4+ count below 200 cells/μl; indicator conditions appear.

Resistance to HIV Infection

  • Initial strong immune response; cytotoxic T lymphocytes (CTLs) suppress viral numbers.

  • Latently infected CD4+ T cells make it impossible to clear infection.

  • Vaccine development is challenging.

Impact of Age and Genetics

  • Older adults and young children are more susceptible.

  • Some exposed individuals remain uninfected due to CCR5 mutation.

  • Long-term survivors have low viral loads and effective CTLs.

Diagnostic Methods

  • Blood is the most common sample; urine and saliva can also be used.

  • Rapid test kits detect antibodies or antigens.

  • Seroconversion (development of detectable antibodies) can take up to 3 months (window period).

  • Virus RNA detected by nucleic acid tests (NATs).

  • Plasma viral load (PVL) measured by PCR to detect viral RNA.

Transmission of HIV

  • Transmitted via: non-sterile syringes/needles, pregnancy/breastfeeding, blood transfusion, organ transplant, unprotected sex.

  • Not transmitted via: food/drink, insect bites, casual touch, clothes/towels, toilet/shower.

Global Epidemiology

  • 39 million infected worldwide (2022).

  • 70% in sub-Saharan Africa; 8.45 million in South Africa.

  • 630,000 deaths worldwide in 2022.

  • Incidence could exceed 1 million cases/year.

  • Key populations: men who have sex with men, people who inject drugs, people in prisons, sex workers, transgender people.

  • More women/girls infected in sub-Saharan Africa.

Preventing and Treating AIDS

Prevention Strategies

  • Use of condoms and discouraging sexual promiscuity.

  • Use of sterile needles.

  • Availability of medications; AIDS is now considered a treatable chronic disease in developed countries.

  • Pre-exposure prophylaxis (PrEP) reduces transmission risk.

Antiretroviral Therapy (ART)

  • Fusion/cell entry inhibitors: Target gp41 region.

  • Reverse transcriptase inhibitors: Nucleoside (NRTIs) and non-nucleoside (NNRTIs).

  • Highly active antiretroviral therapy (HAART): Uses combinations of drugs.

  • Integrase inhibitors: Inhibit HIV integrase.

  • Protease inhibitors: Inhibit viral proteases.

  • Maturation inhibitors: Prevent virus assembly.

  • Tetherins: Tether viruses to cells, preventing release and spread.

Mechanisms of Action: NNRTI vs NRTI

  • NRTIs: Mimic natural nucleosides, are incorporated into viral DNA by reverse transcriptase, causing chain termination.

  • NNRTIs: Bind directly to reverse transcriptase, inhibiting its activity without being incorporated into DNA.

Challenges in HIV Vaccine Development

  • No model of natural immunity to mimic.

  • Lack of suitable research animals.

  • Poor understanding of retrovirus mechanisms.

  • High mutation rate leads to resistant strains.

  • An ideal vaccine would induce immunity before latent reservoirs are established, stimulate CTLs, and be affordable.

Key Equations and Concepts

  • CD4+ T cell count threshold for AIDS diagnosis:

  • Viral load quantification by PCR:

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