EXAM: Basic Virology, Viral Replication, OmpathStudy

Basic Virology, Viral Replication, Prions & Slow Viruses, Poxviruses & VZV High-Yield Revision Notes Institution: Mount Kenya University — School of Medicine & Surgery Unit: MBMM 3300 — Medical Virology and Mycology Level: MBChB Year 3 --- Papers & Examinations Covered Exam Date Paper --- --- --- Main Exam January 2022 MBMM 3300 Paper 1 Main Exam February 2021 MBMM 3300 Paper 2 Main Exam July 2019 MBMM 3300 Paper 2 Main Exam January 2023 MBMM 3300 Paper 2 End of Term CAT December 2020 MBMM 3333 Medical Virology CAT II 2018/2019 MBMM 3233 Medical Virology --- Topics Covered Basic Virology — classification, structure, Baltimore system, viral components and their functions Viral Replication — lytic cycle, lysogeny, growth curve, replication of DNA and RNA viruses Prions and Slow Viruses — structure, diseases, pathogenesis, diagnosis Poxviruses and Varicella-Zoster Virus — structure, diseases, clinical features, vaccines, treatment --- --- Part 1: Basic Virology — Classification and Structure 1. Introduction Basic virology forms the foundation of everything else in the virology course. Without understanding what a virus is, how it is classified, and what its components do, it is impossible to understand pathogenesis, diagnosis, or treatment. At MKU, basic virology appears heavily in MCQs — testing viral classification, the Baltimore system, functions of viral components, and distinguishing features of specific virus families. Several essay questions on viral receptors and spikes and viral pathogenesis also draw directly from this foundational knowledge. --- 2. What is a Virus A virus is an obligate intracellular parasite — it can only replicate inside a living host cell. It is not a cell — it has no organelles, no ribosomes, no cell membrane of its own, and no metabolic machinery. It hijacks the host cell's machinery to replicate. Key features that distinguish viruses from other microorganisms: Contains only one type of nucleic acid — either DNA or RNA, never both Has no ribosomes — cannot synthesize proteins independently Has no mitochondria — cannot generate energy Replication by assembly of pre-formed components — not by binary fission Much smaller than bacteria — range from 20 nm (parvovirus) to 300 nm (poxvirus) --- 3. Viral Structure — Components and Functions The Genome Either DNA or RNA — never both Can be single-stranded (ss) or double-stranded (ds) Can be positive-sense (+) or negative-sense (-) Positive-sense RNA — same sequence as mRNA; can be directly translated by host ribosomes Negative-sense RNA — complementary to mRNA; must be converted to positive-sense first by viral RNA polymerase before translation Can be segmented (multiple separate pieces) or non-segmented (one continuous piece) Segmented genomes — influenza (8 segments), rotavirus (11 segments) Segmentation allows genetic reassortment — basis of antigenic shift in influenza The Capsid Protein coat that surrounds and protects the viral genome Made of repeating protein subunits called capsomeres Two main shapes: Icosahedral — spherical, 20 triangular faces; most efficient use of protein; examples: adenovirus, HSV, poliovirus, papillomavirus Helical — protein subunits arranged in a helix around the genome; examples: influenza (inside envelope), rabies, TMV Complex — neither icosahedral nor helical; example: poxvirus (most complex animal virus) Functions of capsid: Protects genome from nucleases and environmental damage Mediates attachment to host cells (in non-enveloped viruses) Determines antigenicity — capsid proteins are targets of antibodies Facilitates entry into host cell The Envelope Lipid bilayer membrane derived from host cell membrane during budding Present in enveloped viruses — absent in non-enveloped (naked) viruses Contains viral glycoproteins (spikes) inserted into it Functions: Mediates attachment to host cell receptors via glycoprotein spikes Mediates fusion with host cell membrane Target of neutralizing antibodies Clinical significance of envelope: Enveloped viruses are sensitive to: Drying — envelope desiccates Detergents and soap — dissolve lipid envelope Acid pH — destabilizes envelope Heat — denatures envelope proteins This is why handwashing with soap kills enveloped viruses (HIV, influenza, herpes) Non-enveloped viruses are resistant to: Drying, acid, detergents — survive on surfaces, in gut, in water This is why enteroviruses and adenoviruses spread easily via fomites and fecal-oral route The Tegument Layer of proteins between capsid and envelope — unique to herpesviruses Contains viral proteins that are immediately active upon cell entry — before viral gene expression begins Tegument proteins: Shut down host protein synthesis immediately Initiate viral gene transcription Block host antiviral responses early Matrix Proteins Link the envelope to the capsid Important in viral assembly and budding Example: M protein in influenza, paramyxoviruses, rhabdoviruses --- 4. Enveloped vs Non-Enveloped Viruses Feature Enveloped