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Related Concept Videos

Rous Sarcoma Virus (RSV) and Cancer01:03

Rous Sarcoma Virus (RSV) and Cancer

Rous Sarcoma virus or RSV was discovered by F. Peyton Rous in the year 1911 as a filterable transmissible agent that could cause tumors in chickens. He won a Nobel Prize for this discovery in 1966. His experiments clearly demonstrated that some cancers could be caused by infectious agents and led to the discovery of many more cancer-causing viruses in animals as well as humans.
RSV is a retrovirus that contains two copies of a plus-strand  RNA genome. Its genome consists of four main open...
Rous Sarcoma Virus (RSV) and Cancer01:03

Rous Sarcoma Virus (RSV) and Cancer

Rous Sarcoma virus or RSV was discovered by F. Peyton Rous in the year 1911 as a filterable transmissible agent that could cause tumors in chickens. He won a Nobel Prize for this discovery in 1966. His experiments clearly demonstrated that some cancers could be caused by infectious agents and led to the discovery of many more cancer-causing viruses in animals as well as humans.
RSV is a retrovirus that contains two copies of a plus-strand  RNA genome. Its genome consists of four main open...
Mechanisms of Retrovirus-induced Cancers01:51

Mechanisms of Retrovirus-induced Cancers

Retroviruses are RNA viruses that have been shown to cause cancers in diverse species, including chickens, mice, cats, and monkeys. The RNA genomes of these viruses are first reverse-transcribed into single and then double-stranded DNA (dsDNA) copies. This dsDNA called proviral DNA then integrates into the host genome. Subsequently, the host cell transcribes the proviral DNA in concert with the chromosomal DNA. This leads to the production of viral RNA and proteins that assemble at the host...
Mechanisms of Retrovirus-induced Cancers01:51

Mechanisms of Retrovirus-induced Cancers

Retroviruses are RNA viruses that have been shown to cause cancers in diverse species, including chickens, mice, cats, and monkeys. The RNA genomes of these viruses are first reverse-transcribed into single and then double-stranded DNA (dsDNA) copies. This dsDNA called proviral DNA then integrates into the host genome. Subsequently, the host cell transcribes the proviral DNA in concert with the chromosomal DNA. This leads to the production of viral RNA and proteins that assemble at the host...
Cancer Vaccines01:30

Cancer Vaccines

Cancer treatment vaccines are a rapidly evolving field that offers a promising approach to immunotherapy. Unlike traditional vaccines that prevent diseases, cancer treatment vaccines are designed to treat existing cancers by stimulating the immune system to recognize and attack cancer cells.
Cancer vaccines come in two categories: preventive (prophylactic) and treatment (active). Preventive vaccines, such as the Human Papillomavirus (HPV) vaccine, protect against viruses that cause certain...
Cancer Prevention02:59

Cancer Prevention

Several factors can increase the risk of cancer in an individual. About 50% of cancer cases can be prevented by adopting a healthy lifestyle, regular exercise, eating healthy, and following a modest cancer prevention diet. Epidemiological studies have consistently shown that populations with vegetable and fruit-rich diets have reduced the incidence of cancer. On the other hand, populations who have a diet rich in animal fat, red meat, junk food, or high calories are predisposed to cancer.
Some...

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Related Experiment Video

Updated: May 21, 2026

RNAscope for In situ Detection of Transcriptionally Active Human Papillomavirus in Head and Neck Squamous Cell Carcinoma
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RNAscope for In situ Detection of Transcriptionally Active Human Papillomavirus in Head and Neck Squamous Cell Carcinoma

Published on: March 11, 2014

Cancer associated human papillomaviruses.

Margaret E McLaughlin-Drubin1, Jordan Meyers, Karl Munger

  • 1Division of Infectious Diseases, Brigham and Women's Hospital and Department of Medicine, Harvard Medical School, Boston, MA 02115, USA.

Current Opinion in Virology
|June 5, 2012
PubMed
Summary

Human papillomaviruses (HPVs) cause various cancers, including cervical and skin cancers. This review explores how HPVs interact with host cells to replicate and cause disease.

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Use of Interferon-γ Enzyme-linked Immunospot Assay to Characterize Novel T-cell Epitopes of Human Papillomavirus
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Use of Interferon-γ Enzyme-linked Immunospot Assay to Characterize Novel T-cell Epitopes of Human Papillomavirus

Published on: March 8, 2012

Related Experiment Videos

Last Updated: May 21, 2026

RNAscope for In situ Detection of Transcriptionally Active Human Papillomavirus in Head and Neck Squamous Cell Carcinoma
10:26

RNAscope for In situ Detection of Transcriptionally Active Human Papillomavirus in Head and Neck Squamous Cell Carcinoma

Published on: March 11, 2014

Use of Interferon-γ Enzyme-linked Immunospot Assay to Characterize Novel T-cell Epitopes of Human Papillomavirus
13:41

Use of Interferon-γ Enzyme-linked Immunospot Assay to Characterize Novel T-cell Epitopes of Human Papillomavirus

Published on: March 8, 2012

Area of Science:

  • Oncology
  • Virology
  • Cell Biology

Background:

  • Certain human papillomaviruses (HPVs) are primary causes of cervical carcinoma and contribute to other anogenital and oral cancers.
  • Distinct HPV groups are linked to non-melanoma skin cancers, particularly in immunocompromised individuals or those with genetic predispositions following UV exposure.

Purpose of the Study:

  • To review the complex interactions between HPVs and host cells during infection.
  • To highlight the mechanisms HPVs employ to subvert cellular processes for their replication.
  • To compare and contrast the biological strategies of different HPV groups in establishing persistent infections.

Main Methods:

  • Literature review of existing research on HPV biology and pathogenesis.
  • Analysis of viral proteins involved in host cell manipulation.
  • Examination of cellular responses to HPV infection and viral evasion strategies.

Main Results:

  • HPVs hijack host DNA synthesis machinery for viral genome replication.
  • Viral proteins maintain differentiated epithelial cells in a replicative state, disrupting normal cell signaling.
  • HPVs inactivate cellular tumor suppressor pathways to ensure persistent and productive infections.

Conclusions:

  • HPVs establish persistent infections by intricately manipulating host cell machinery and signaling pathways.
  • Understanding the interplay between HPVs and host cells is crucial for developing targeted therapies.
  • Biological similarities and differences exist among HPV groups, influencing their oncogenic potential and disease presentation.