Pathogenesis of Viral

Infections
 Virus Spread And Disease (Pathog.)

Skin, Mucous Membrane: Rabies, HSV, HPV, Arthropod bite

Alimentary: Entero Virus, Rota Virus

Respiratory: Orthomyxo Virus, paramyxovirus

Urogenital: HSV2, HPV CMV, HBV, HCV, HIV

Conjunctiva: Adeno, HSV, Entro 70, Cox A24

Saliva: HSV, EBV, CMV

Congenital: Rubella, CMV, Varicella

Blood: HBV, HCV, HIV, Entro Virus, Arbo Virus

Neural: Rabies, HCV, VZV
 Pathogenesis of Viral Infections

Effects of Viruses on Cells

Way of virus spread in the body and cause
disease

Immune Response against virus infections

Virus shedding outside the cells

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 Effect of Viruses on Cells

Cytocidal Infection

Steady-state Noncytocidal Infection (Persistent Infection)

Cellular Transformation

A. Cytocidal Infection
1. Cell death and histological appearance of characteristic CPE
E.G. Picorna, herpes
2. Biochemical changes in infected cells
3. Host protein shut down by virus protein synthesis i.e.
Picornaviruses, Herpes Viruses
4. Viral proteins or Virions form inclusions
5. Infected cells usually swell 4
 Effect of Viruses on Cells (Contd.)
B. Steady-State Persistent Infection:
1. Infected cells:
 Produce and release virus but no CPE
 Can grow and divide but not killed
2. Does not occur with DNA viruses
3. Occur with several RNA viruses (Lassa virus, Retoviruses,
Rubella, some paramyxoviruses)
4. Virus released by cell budding
5. Demonstrated by: Hemadsorption, direct IFT

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 Effect of Viruses on Cells (Contd.)
C. Cellular Transformation:
1. Viruses produce tumors in animals can transform cell culture
2. Virus DNA into host DNA, alter growth and morphology
3. Chrosomal abnormalities
4. New virus Ag and DNA production
5. Ex.: Adeno, HPV, HSV, EBV, HBV (retroviruses: Sarcoma
virus, HTLV1,2)

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Inclusion Bodies (CPE)
1. Most characteristic viral morphological changes
2. Single or multiple, large or small
3. Round or irregular, intranuclear or intracytoplasmic, acidophilic
or basophilic
4. Intracytoplasmic inclusion (ICI) (most characteristic):
Poxviruses, paramyxo, Rabies
5. Intranuclear inclusion (INI): Herpes, Adeno
6. INI and ICI: CMV, Measles
7. Identification of INI and ICI: EM, IFT, H & E stain
8. Most commonly due to viruses, but not diagnostic

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Inclution bodies
A - Vaccinia
B - HSV
C - Reovirus
D Rabies
F Measles, CMV
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Inclusion Bodies: The site of VIRAL
Multiplication and Protein Synthesis

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Giant Cell Formation
(Syncetium)

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 Recovery From Infection
1. Humoral (B-cells): Abs production
2. CMI (T-cells): T lymphocytes
3. Essnetial host defense mechanism:
 Macrophages
 Phagocytes
 Cytokines (IFN, IL)
 Natural Killer cells (NK)
 Cytotoxic T cells (CD 8 lymphocyte)
 Complement
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 Recovery From Infection (Pathog.)
1. Humoral Immunity:
Abs affects only extra cellular viruses
 IgM, IgG: control the viremic stages of infection
 IgA: protect epithelial surface
 Prevent reinfection (prevent binding of virus to its
receptor or viral entry)
2. CMI:
Effective against intracellular viruses
 Its action involve cytotoxic T cells (CD8) which destroy
infected cells
 Limit the spread of secondary infection 12
 Recovery From Infection (Pathog.)
3. Essential Host Defense Mechhanism:
 Macrophages: secrete cytokines to activate T cells
 Phagocytes: destroy (Ab-complement-virus) complex)
 Cytokines (IFN, IL):
 IFN: Stimulate body immunity, inhibit viral translation
 Interleukin: stimulate Ab secretion, activate T cells
and NK cells
 Natural killer (NK) cells: lysis of infected cells
 Cytotoxic T cells (CD8 lymphocyte): lysis of infected
cells
 Complement: damage enveloped viruses
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