10b: CPEs Flashcards
What are Cytopathic effects, CPEs?
- alterations in the morphology of cells due to virus infection
- usually degenerative processes
- mainly observed in cell cultures
- direct damage of viruses on cells
- CPE may occur ondependently or jointly
- Different viruses may cause similar CPE
- CPE may vary according to the host cell
What can be direct damages of viruses on the cells?
- toxic effec of adsorption (i.e adenoviruses)
- virus proteins inhibit cellular translation (i.e herpes-, pox-, togaviruses)
- early proteins inhibit cellular nucleic acid transcription and replication (i.e herpes, adenoviruses)
- viral proteins or virions are deposited in the cells
- viral proteins damage the cytoplasmic membrane permeability - osmotic changes (i.e herpesviruses)
- cytoskeleton depolymerisation (i. e herpes-, paramyxoviruses)
- expression of fusion proteins (i.e herpes-, paramyxoviruses)
CPEs: tools for the detection of virus multiplications in vitro:
- usually investigated by light microscopy (100-400 x magnification)
- some CPEs are visible in unstained cells
- staining: HE, Giemsa gives more detailed information.
BUT: not all virus infections result in CPE
Why does not all virus infections result in CPE?
- the cytopathic character of a virus strain may change due to mutations (i.e BVDV)
- the CPE is not always connected to the pathogenicity of the virus:
- -> ie: CSF - no CPE but pathogen
- -> ie: Spumaviruses - obvious CPE but orphan
What does MOI mean?
that the appearance of the CPE is Influenced by Multiplicity of Infections (MOI)
- the most characteristic CPE is seen by low MOI (<0.1)
What does it mean that the CPE may vary according to the host cell?
- CPE alone is usually not pathognomic
- CPE is important character for the identification of the virus.
What are the main types of CPEs?
- Inclusion body formation
- Cell rounding
- Syncytium formation
- Lumpy cell nucleus
- Cell vacuolisation
- hemadsorption
What are the types of Inclusion body formation?
- Intranuclear inclusion bodies
- Intracytoplasmic inclusion bodies
Where are Inclusion body formation seen?
- at the site of assembly of nucleocapsid –> virus deposition
- seen in stained cells (of cell cultures or organ sections)
- -> homogenous staining
- -> surrounded by halo - shrinkage after fixation
What causes Intranuclear inclusion bodies?
- In the nucleus replicating DNA viruses (i.e parvo-, papilloma-, polyoma-, adeno-, herpesviruses)
- sometimes caused by RNA viruses (i.e orthomyxo-, paramyxo-, arteri-, bornaviruses)
- Cowdry-A, Cowdry-B types depends on the state of the synthesis of macromolecules
How are the Intranuclear inclusion bodies stained?
- Basophyl: i.e parvo
- Amphophyl: i.e adeno
- Eosinophyl: i.e herpesviruses
What causes Intracytoplasmic inclusion bodies?
- usually caused by RNA viruses
- DNA viruses replicating in the cytoplasm (poxviruses, ASFV)
- eosinophil, rarely basophyl (poxviruses)
- pathognomic: Negri bodies (rabies), Guarnieri bodes (pox)
How are Intracytoplasmic inclusion bodies stained?
- eosinophil, rarely basophyl (poxviruses)
- pathognomic: Negri bodies (rabies), Guarnieri bodes (pox)
Cell rounding:
- one of the most frequent CPE
- cytoskeleton depolymerisation
- loss of electrolytes
- unstained: double refraction, detachment, shrinkage
- stained: intensive staining
Syncytium formation:
- caused exclusively by enveloped viruses (alphaherpes-, paramyxo-, pneumo-, coronaviruses)
- fusion proteins (F) on the surface of the virus
- giant cells with many nuclei: polykaryocytes, syncytia.
- in tissue sections multinucleated giant cells may be seen: usually lymphatic cells, results of impared cellular division.
