Download herpes simplex virus

Viral Infection
Detection
Viral Infection Detection
Clinical examinations & findings
Antibody detection
Electron Microscopic: SEM & TEM
Molecular assays: PCR
Detection of viral receptors
Example: Hemagglutination & Hemagglutination inhibition
Culture
Plaque formation (PFU, Pock)
The Culture of Viruses
1. laboratory animals
2. Embryonated eggs
3. Cell lines (Tissue cultures)
Primary cell culture
Diploid cell lines
Continuous cell lines
Cytopatic effects
(CPEs)
Cytopatic effects (CPEs):
Cell lyses (degeneration)
Aggregation
Malignant transformation
Giant cells
Cell rounding
Viral gene expression
Loss of attachment (to culture dish)
Cell-Cell fusion (Syncytial cells)
Inclusion body: Negri body
Rabies Negri bodies
Syncytial cells by Respiratory syncytial
virus (RSV)
herpes simplex virus (HSV) type 1-infected primary rabbit kidney cells
CPE: rounding and detachment of cells
Adenovirus beta galactosidase
Viral genetics
Virus - Virus interactions
Viral cancers
Different interactions between two
different viruses in a cell
Recombination (based on Crossing over)
- between HSV1 & HSV2
Reassortment
- between Influenza viruses
Complementation
- Rescue of a lethal mutant with a defined genetic sequence
of other virus
Transcapsidation
- Pseudoviruses
Cell transformation
Changes in cellular growth, cellular morphology, antigenic
compounds.
Oncogenic viruses can be carcinogen (causing malignant
tumors) and make cells to transform.
Tumor viruses
Why some viruses are considered the causative of tumors?
- Biological criteria for causal association of viruses with
tumors:
The presence of virus in tumor tissues
The presence of virus before disease onset
Viral persistence
The location of virus at appropriate sites
Prevention of the disease by prevention of viral
infection
Human Oncogenic viruses
Human Oncogenic RNA viruses
 Retroviruses: HTLV-1 & HTLV-2, HIV: Kaposi’s sarcoma
Human Oncogenic DNA viruses
 Human Hepatitis B virus: Hepatocellular carcinoma
 Herpesviruses: Epstein-Barr virus: Burkitt’s Lymphoma/
Epstein-Barr virus: Nasopharyngeal Carcinoma
 Herpesviruses: Herpes Simplex virus Type 2: Cervical
intraepithelial neoplasia
 Herpesviruses: Human Cytomegalovirus: Cervical tumors/
 Human Papillomaviruses: types 18, 16, 33: Cervical cancer
Viral and hast genes involved
in cancers
Virus:
Promoter genes (viral oncogenes= v-onc )
Host:
Tumor Repressor Genes
Oncogenes (cellular oncogenes= c-onc)
Tumor Repressor Genes
(Anti-oncogenes)
They are normally oncogene regulators.
If repressed (e.i. by a virus promoter)
 Activating the relevant oncogene  Causing oncogene
products Cell transformation
Cellular Oncogenes
(c-onc genes)
Normally inactivated.
If disregulated or mutated, then causes transformation in the
cell by oncogene products.
Example:
Retinoblastoma (Rb) gene is one of these tumor repressor
genes which regulates the pass of the cells to S stage of the
cell cycle. Mutation of Rb gene by some viral promotors
transforms the cell.
Growth factors
Signaling proteins
DNA binding proteins and other regulatory proteins
Cellular receptors