NAJRAN UNIVERSITY College of Medicine

1. NAJRAN UNIVERSITY College of Medicine Microbiology &Immunology Course Lecture No. 19 By Dr. Ahmed MoradAsaad Associate Professor of Microbiology

2. Virus-cell interactions • Replication • Viruses multiply only in living cells • The replication cycle consists of the following steps: • 1- Attachment (adsorption) • Viral replication starts with interaction of the virus with specific receptors on the cell surface • Receptor molecules differ for different viruses (viral tropism) • Antiviral antibodies can inhibit this process

3. 2- Penetration (Engulfment) • Non-enveloped viruses penetrate the host cell by a process of phagocytosis forming a cytoplasmic vacuole that will dissolve releasing the nucleocapsid into the cytoplasm • Enveloped viruses penetrate the cell by fusion of the viral envelope with the cell membrane releasing the nucleocapsid into the cytoplasm

4. 3- Uncoating • It is the physical separation of viral nucleic acid from its capsid • 4- Eclipse phase • During this period (some hours), several enzymes are produced by the host cells under control of viral genome • The cell metabolism is now directed to the synthesis of new viral particles • This phase ends with the formation of the infectious virus

5. 5- Assembly • Viral nucleic acid becomes surrounded by its capsid to form the mature virion (nucleocapsid) • 6- Release • Release of viruses to extracellular environment either by cell lysis or by budding through cell membrane leaving the host cell intact • Enveloped viruses mature by a budding process

6. Inclusion bodies: • They are virus specific structures produced in the course of viral replication. (Areas of viral assembly) • Inclusion bodies may be: • Intranuclear: e.g. herpes viruses • Intracytoplasmic: e.g. pox viruses • In both: e.g. measles virus • Their presence in the cells is diagnostic of: • Negri bodies in Rabies • Guarnieri bodies in small pox • Torr’s bodies in yellow fever

7. Pathogenesis of viral infections: • The outcome of virus-cell interaction may be: • Cell death or lysis • Abortive infection: No synthesis of new viral particles. Viral replication is blocked • Latent infection: The viral genome persist inside the host cell for a period. There will be flare-up of clinical disease • Transformation: The host cell will acquire new characters leading to rapid growth and malignancy

8. Viral infections may be: • Superficial: short incubation period – No invasion. E.g. Influenza viruses, Rota virus • Systemic: After viral entry, it will spread to local lymphoid tissues followed by viraemia and spread to target organs. • Examples: • Skin & M.M. in measles and chicken pox • Liver in hepatitis viruses • Meninges in enterovirus meningitis

9. Persistent: The virus will persist for a long period. Three types of persistent viral infections: • 1- Chronic infection: leading to chronic diseases as in HBV and HCV • 2- Latent infection: The virus persists silent for a period of time with intermittent flare-up. E.g., measles • 3- Slow virus infection: A very long incubation period, gradual onset and progressive course. E.g., AIDS