10. Virus-Host Interaction

8/7/2019 10. Virus-Host Interaction

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VIRUS- HOST INTERACTION

y Viruses: obligate intracellular parasite- Depend on host cells at ALL stages of infectious stages

y Different viruses may affect the same or different host cell metabolism-

Virus-host interactions are DIVERSE and COMPLEX

Types of virus-host interactions

1. Productive infections- Cytocidal infections- Productive transformation- Persistence

2. Non-productive infections- Apoptosis- Non-productive transformation- Latency

Productive Infections

y When viral progeny ate produced from infected cellsy Progeny: from very few to thousands of infectious particlesy Steps in a typical productive viral infection:-

1. Adsorption (attachment)2. Penetration (uptake)3. Viral disassembly (uncoating)4. Synthesis of viral components5. Assembly of progeny virus particles6. Release of virions

Cytocidal/Lytic

y When host cells caused to be lysed when progeny virions releasedy Cell culture: Cytopathic Effect (CPE)y CPE: Virus-induced damage to the cell that alters it microscopic appeatance

e.g. Poliovirus lysis

Smallpox virus cells rounded up (ballooning)

Adenovirus clumping of cells

Influena virus cells rounded up

Etc.

y Host cells killed!(I didnt type out Lytic growth cycle. Because Pak Nasa said: No need lah)

Productive Transformation

y Host cells not killed (lysed) but undergo NEOPLASTIC TRANSFORMATIONy Entire genome integrates into that of host cells


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y Expressing ONCOGENESy Host cells transformed to a state of uncontrolled cell divisiony Continuous release of infectious viral progeny usually by buddingy Examples: RNA tumous (oncogenic) viruses

- Human T cell leukemia virus (HTLV-1 and 2)- Sarcoma viruses (cats, chicken)- Mammary tumour viruses (mice)

y Persistence- Infected cells and virus co-exist over a long period of time:

Few weeks to years (or even for a whole lifetime)

- Exact mechanism (??? Not known, yet)- DI (Defective interfering particles)

Temperature sensitive mutants (ts mutants) and IFN all implicated

- E.g. Lympocytic choriomeningitis virus in mouse (LCM)NON PRODUCTIVE INFECTIONS (ABORTIVE)

y The intial stages: same as for productive viral infectionsy Then, non-productie infections can have different courses-

- Apoptosis- Non-productive transformation- Latency

y May be due to a block on one stage of replication cycley Or viral genome may be defective

= Replication cannot be completed

y Viral genome may be too smalle.g. Parvoviridae family needs second helper virus such as Adenoviruses

y Or due to mutationAPOPTOSIS

y Early viral replications steps -? Trigger host cell apoptotic response (programmed celldeath)

= Host and virus : no propagation

y Example: Vaccinia virus in Chinese hamster ovary cells- Cell rounding + condensation of chromatin + fragmentation of DNA

= Blebbing of cell membrane -> break up -> apoptotic bodies

NON-PRODUCTIVE TRANSFORMATION

y Virus infects celly Viral oncogene integrate with cell DNA -> transformation of celly Transformed cells DO NOT yield infectious progeny virus (= non-productive)y E.g Papillomavirus (wart viruses) ~ 77 types

Some causally involved in


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- Canccer of cervix- Cancer of anogenital region

LATENCY

y Virus 0> primary infection -> Progeny (productive)Then -> secondary latent infection (usually neural cells for life)

y Viral genome remains intact during latency in nucleus of host celly Can reemerge throughout life (especially when immunity )y E.g Herpex Simplex (HS)

Herpes Zoster (HSV) chickenpox and shingles

Epstein-Barr virus (EBV) infectious mononucleosis, Burkitts lymphoma and

nasopharyngeal carcinoma.

y (HSV also known as Kayap in Malay)TRANSFORMATION

y Type of virus-cell interactiony Properties of cells change dramaticallyy Transformed cells have similar properties to tumour cellsy Only members of SOME virus families are able to transform cells

Vis

- Herpesviruses- Adenoviruses- Hepadnaviruses- Papovaviruses- Poxviruses

y Rare event: 1 in 10^5 cells infectedy Characteristics of transformed cells

- Loss of contact inhibition of growth- Less requirement for serum factors- Indefinite number of cell divisions- Viral antigens expressed- Fibronectin absent- Fetal antigens found- Induction of tumours in experimental animals

Portsofentry the surfaces:

- Skin- Mucosa- Oropharynx and GIT- Respiratory tract- Urogenital tract

SKIN


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Breached through (injections via):-

y Transcutaenousy Intervenous

Vectors (usually insects. Arthropod-borne/ARBO)

y Arboviruses- Togavirus (EEE,WEE, VEE)- Flavivirus (DG, JE, YF)- Bunyavirus (Crimean Congo HF)- Reovirus (Colorado tick fever)- Rhabdovirus (Kotonkan obodhiang)

y Bite- Intramuscular- Rhabdovirus

y Injection (IV drug user, iatrogenic)- Hep B, C, D- CMV- HIV

y STD- Papilloma- HSV- Hep B- HIV

Skin, mucous membranes, oral and genital fluids, semen & milk

y Few from skin lesions- HSV (labial transmission- HV (rare: zoster -> chickenpox)- Papillomaviruses- Molluscum contagiosum- Ebolavirus

y STD: HS type 2 & Papillomavirusesy Rabies, mumps and EBC replicate in salivary glands -> discharged into saliva -> oral

cavityy Semen Hep B and HIVy Colostrum & Milk CMV, Mumps and Rubellay Blood

- Hep B,C,D- HIV- HTLV-1, HTLV-2- CMB


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y Arboviruses insecty CMV urine -> important spread in young children

Mucosa

Oropharynx and GIT

y Enteric virusesy Togavirus (small & large intestine)y Hepatitis Ay Poliovirus (replication : lymphoid tissue)y Echovirus

Lower GIT (anal intercourse)

y Hepatitis By Herpes Simplexy H

IV

Respiratory Tract

y Rhinovirus (>100 serotypes. They dont offer cross protection)y Myxovirusesy Adenovirusesy Herpesvirusesy Poxviruses

Eye

y Herpes simplexy Herpes Zostery Adenovirus

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10. Virus-Host Interaction