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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

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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...
lncRNA - Long Non-coding RNAs02:39

lncRNA - Long Non-coding RNAs

In humans, more than 80% of the genome gets transcribed. However, only around 2% of the genome codes for proteins. The remaining part produces non-coding RNAs which includes ribosomal RNAs, transfer RNAs, telomerase RNAs, and regulatory RNAs, among other types. A large number of regulatory non-coding RNAs have been classified into two groups depending upon their length – small non-coding RNAs, such as microRNA, which are less than 200 nucleotides in length, and long non-coding RNA (lncRNA)...
lncRNA - Long Non-coding RNAs02:39

lncRNA - Long Non-coding RNAs

In humans, more than 80% of the genome gets transcribed. However, only around 2% of the genome codes for proteins. The remaining part produces non-coding RNAs which includes ribosomal RNAs, transfer RNAs, telomerase RNAs, and regulatory RNAs, among other types. A large number of regulatory non-coding RNAs have been classified into two groups depending upon their length – small non-coding RNAs, such as microRNA, which are less than 200 nucleotides in length, and long non-coding RNA (lncRNA)...

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Noncoding RNAs produced by oncogenic human herpesviruses.

Sankar Swaminathan1

  • 1University of Florida Shands Cancer Center, Gainesville, Florida 32610, USA. sswamina@ufl.edu

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Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV) are linked to human cancers. These viruses encode RNAs, including microRNAs, that play roles in viral replication, immune evasion, and oncogenesis.

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Area of Science:

  • Virology
  • Oncology
  • Molecular Biology

Background:

  • Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV) are human herpesviruses causally linked to various cancers, including lymphomas and epithelial malignancies.
  • Both viruses establish lifelong latency in B lymphocytes and encode proteins and noncoding RNAs crucial for host cell transformation and immune system evasion.

Purpose of the Study:

  • To explore the role of noncoding RNAs, particularly microRNAs, encoded by EBV and KSHV in viral pathogenesis and oncogenesis.
  • To highlight the conserved nature and potential fundamental importance of these viral RNAs in the viral life cycle.

Main Methods:

  • Review and synthesis of existing literature on EBV and KSHV biology, focusing on their encoded noncoding RNAs.
  • Analysis of conserved RNA elements and their expression patterns in various clinical settings.
  • Examination of identified cellular and viral gene targets of viral microRNAs.

Main Results:

  • EBV and KSHV express abundant noncoding RNAs, including nuclear EBER RNAs and recently identified microRNAs, during latent and lytic infections.
  • Viral microRNAs have been shown to target both viral and cellular genes, influencing immune response modulation and oncogenesis.
  • The complex regulatory network of viral microRNAs and their host targets suggests significant implications for disease development.

Conclusions:

  • Noncoding RNAs, especially microRNAs, are critical components of the EBV and KSHV life cycles, contributing to their oncogenic potential.
  • Further research into viral microRNA targets and interactions is essential for understanding their roles in cancer and developing therapeutic strategies.
  • The conserved nature of these viral RNAs underscores their fundamental importance in herpesvirus-mediated diseases.