MKU Medical Virology Exam Guide: HIV, CMV, Vaccines & More –

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 Q