Ace your MKU Medical Virology exams! This study guide covers past paper questions on HIV, CMV, vaccination, viral encephalitis & more with concise answers.
Medical Virology — Study Guide Mount Kenya University MBMM 3300 School of Health Sciences This guide covers all examined topics in Medical Virology as tested across MKU past papers and CATs from 2017/2018 to 2021/2022. Each section presents the exact exam question followed by concise point-form answers structured for quick revision. Questions on HIV enzymes, vaccination, CMV, and viral encephalitis appear in nearly every sitting — prioritise these. Topics examined in both main papers and CATs carry the highest weight. Papers referenced: 2021/2022 2018/2019 2017/2018 Main Exams CAT Medical Virology 2018/2019 CAT Medical Virology December 2020 --- Topics Covered 1. Attenuated Vaccine 2. OPV vs IPV 3. Basic Principle of Vaccination 4. Active vs Passive Immunization 5. Interferon Mechanism 6. Herpes Simplex Virus 7. Viral Receptors and Spikes 8. Reverse Transcriptase and Integrase in HIV 9. Cytomegalovirus Pathogenesis 10. CMV in Congenital Infections 11. Adenovirus 12. Rabies 13. Viral Encephalitis 14. Influenza Antigenic Changes 15. Haemorrhagic Fever Viruses 16. Prions 17. Normal Cell vs Tumour Cell 18. COVID-19 Contact Tracing --- 1. Attenuated Vaccine Question: A child born in Muranga was vaccinated with an attenuated vaccine. Explain briefly how it is supposed to protect the child from the particular viral infection - Attenuated vaccine contains live but weakened virus — unable to cause disease but able to replicate - Replication stimulates both humoral and cell-mediated immunity - B cells produce specific antibodies (IgM initially, then IgG) - Memory B and T cells are generated and persist long-term - On future exposure to virulent virus, a rapid anamnestic (secondary) immune response is mounted - Antibodies neutralise virus before it causes disease - Produces long-lasting immunity , often lifelong, mimicking natural infection --- 2. OPV vs IPV Question: OPV and IPV are attenuated and inactivated vaccines respectively. Describe how they were produced and explain why some countries prefer IPV over OPV Production: - OPV (Oral Polio Vaccine / Sabin) — poliovirus passaged repeatedly through non-human cell cultures at low temperatures until virulence is attenuated; virus is alive but weakened - IPV (Inactivated Polio Vaccine / Salk) — wild poliovirus grown in culture then inactivated with formalin ; virus is killed and cannot replicate Why some countries prefer IPV: - OPV can revert to virulent form — causes Vaccine-Associated Paralytic Poliomyelitis (VAPP) - IPV cannot revert — no risk of VAPP - IPV preferred in countries where wild polio has been eliminated - OPV still preferred where polio is endemic — cheaper, oral administration, induces gut mucosal immunity --- 3. Basic Principle of Vaccination Question: What is the basic principle of vaccination? How do vaccines prevent microbial infections? Basic principle: - Based on immunological memory - Expose the immune system to an antigen without causing disease - Primes the immune system to respond rapidly and powerfully upon real infection How vaccines prevent infection: - Vaccine antigen is processed by antigen-presenting cells (APCs) - APCs activate T helper cells (CD4+) - T helper cells stimulate B cells to differentiate and produce specific antibodies - Cytotoxic T cells (CD8+) are also activated — important for intracellular pathogens - Memory B and T cells persist long-term in lymphoid tissue - On natural exposure: memory cells mount a fast, strong secondary immune response - Virus is neutralised before clinical disease can develop --- 4. Active vs Passive Immunization Question: Explain the mechanism of active immunization and how it differs from passive immunization Active immunization: - Host's own immune system is stimulated by an antigen - Takes days to weeks to develop full immunity - Produces long-lasting memory cells and antibodies - Includes live attenuated, killed/inactivated, subunit, and toxoid vaccines Passive immunization: - Preformed antibodies are transferred directly to the host - No immune stimulation or memory cell generation - Provides immediate but short-lived protection — antibodies degraded over weeks to months - Examples: immunoglobulin injections, maternal antibodies passed to neonate, anti-rabies immunoglobulin post-exposure --- 5. Interferon Mechanism Question: Explain how interferon helps virus-infected cells fight back the infection - Virus-infected cell produces Type I interferons (IFN-alpha and IFN-beta) in response to viral dsRNA - Interferons are secreted and bind receptors on neighbouring uninfected cells - Triggers the JAK-STAT signalling pathway - Upregulates antiviral proteins: Protein kinase R (PKR) , RNase L , Mx proteins - PKR phosphorylates eIF-2alpha — halts protein synthesis , preventing viral replication - RNase L degrades viral RNA - Interferons activate NK cells and macrophages - Upregulate MHC class I expression — enhances recognition and destruction of infected cells by cytotoxic T cells - Net result: viral spread is slowed while adaptive immunity develops --- 6. Herpes Simplex Virus Question: Name the portal of entry of HSV1 and HSV2. Mention 3 diseases caused by herpes simplex viruses Portal of entry: - HSV-1 — oral mucosa, skin (especially face), respiratory tract - HSV-2 — genital mucosa and skin; transmitted at birth (neonatal herpes) Diseases caused: - Oral herpes / cold sores (herpes labialis) — HSV-1 - Genital herpes — HSV-2 (occasionally HSV-1) - Herpes encephalitis — HSV-1; most common cause of sporadic viral encephalitis - Neonatal herpes — HSV-2; acquired during delivery - Herpetic keratoconjunctivitis — HSV-1 - Herpetic whitlow — infection of the finger --- 7. Viral Receptors and Spikes Question: Discuss in detail the clinical importance of viral receptors/spikes. You may give specific examples to support your answer - Viral surface proteins (spikes) mediate attachment to specific host cell receptors — the essential first step of infection - Determine host range and tissue tropism — explain why certain viruses infect specific organs - Key examples: - HIV gp120 binds CD4 and CCR5/CXCR4 co-receptors — tropism for T helper cells and macrophages - Influenza haemagglutinin (HA) binds sialic acid on respiratory epithelium - SARS-CoV-2 spike protein binds ACE2 receptors on lung and gut epithelium - Rabies virus binds nicotinic acetylcholine receptors at neuromuscular junctions — explains neurotropism - Rhinovirus binds ICAM-1 on nasal epithelium - Receptors are prime targets for vaccine development e.g. spike protein vaccines for COVID-19 - Receptors are targets for antiviral drugs e.g. fusion inhibitors, receptor blockers - Receptor binding triggers conformational change enabling membrane fusion and viral entry - Mutations in host receptor genes can confer natural resistance e.g. CCR5-delta32 mutation — resistance to HIV - Understanding receptors explains species barriers and zoonotic spillover events --- 8. Reverse Transcriptase and Integrase in HIV Question: Discuss the importance of reverse transcriptase and integrase in the pathogenesis of HIV infection. Explain how antiretroviral drugs targeting these enzymes are selectively toxic Reverse Transcriptase (RT): - HIV carries its genome as single-stranded RNA - RT converts viral RNA → complementary DNA (reverse transcription) - Produces RNA-DNA hybrid; RT's RNase H activity then degrades the RNA strand - RT synthesises second DNA strand → double-stranded DNA (dsDNA) - Without RT, HIV cannot replicate or integrate into host genome - RT has high error rate with no proofreading — generates mutations leading to drug resistance and immune evasion Integrase: - Viral dsDNA is transported to the nucleus - Integrase catalyses integration of viral DNA into the host chromosome → forms provirus - Provirus is permanent — persists for the life of the cell - Allows latent infection and viral reservoir formation in resting CD4+ T cells - Upon cell activation, host cell transcribes proviral DNA producing ne