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7 views

113lecture1906slides

Uploaded by

Md. Murtuza kamal
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PDF, TXT or read online on Scribd
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Microbiology - Viruses

Viruses and Cancer


Latent Viral Infection
Prions

Oncogenesis
• Cancers develop when cells are released from
normal control on their division
– This may also involve release from the tissue in which
the transformed cells arose, leading to metastasis
– Cancers usually arise from mutation of proto-
oncogenes, which encode regulatory proteins
• Viral infection may increase the risk of malignant
transformation if
– Viral gene products influence mutation frequency in
host cells
– Viral genomes disrupt critical host genes

Human Viruses and Cancer


• No human virus causes cancer in more than
a small minority of infected persons
• Nevertheless, viral infection is the second
leading known cause of human cancers
• Human oncogenic viruses belong to several
different families
• A common feature is integration of the viral
genome into the host cell genome at some
point in viral multiplication
Human Papillomavirus (HPV)
• Papovavirus family
• Very common sexually transmitted
infection
• Certain genotypic forms show a very strong
association with cervical cancer

Epstein-Barr Virus (EBV)


• Herpesvirus family
• Extremely common virus infection; estimated 80% of
Americans show evidence of exposure
• Most commonly associated with infectious mononucleosis
• Increases risk for Burkitt’s lymphoma and nasopharyngeal
carcinoma
Hepatitis B Virus (HBV)
• Hepadnavirus family
• Transmitted sexually and by other close contact
• Of greatest concern among bloodborne pathogens
• May be controlled by vaccination
• Associated with increased risk for hepatic carcinoma: liver
cancer

HTLV I
• Human T lymphotropic virus, a retrovirus (same family as
HIV)
• Associated with increased risk for certain lymphomas and
leukemias

Latent Infection
• Characteristic of Herpesviruses
– Herpes Simplex Viruses I and II (HSV)
– EBV
– Cytomegalovirus (CMV)
• After initial infection, the viral genome may
persist in host cells without active production of
virions
• This prevents host defense from “seeing” the
virus
• Physiological changes may trigger reactivation of
active multiplication
Prions
• Infectious proteins
• Misfolded form of a normal cell protein, PrP
• May cause normal copies to likewise misfold; this is how
a prion “multiplies”
• Most common human prion disease is Creutzfeldt-Jacob
Disease (CJD)

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