Viral Infections: Negative Regulators of Apoptosis and Oncogenic Factors

A V Zamaraev1, B Zhivotovsky1,2, G S Kopeina3

  • 1Faculty of Basic Medicine, Lomonosov Moscow State University, Moscow, 119192, Russia.

Biochemistry. Biokhimiia
|November 17, 2020
PubMed

Insights

Viruses can disrupt programmed cell death (apoptosis) to cause cancer. This review explores how viruses suppress apoptosis, aiding tumor development and disease progression.

Area of Science:

  • Oncology
  • Virology
  • Cell Biology

Background:

  • Disruption of programmed cell death (apoptosis) is linked to diseases like cancer.
  • Persistent viral infections are implicated in the development of various cancers.
  • Oncogenic viruses interfere with cellular apoptosis pathways.

Purpose of the Study:

  • To review mechanisms by which viruses suppress apoptosis.
  • To elucidate the role of viral apoptosis suppression in oncogenesis.

Main Methods:

  • Literature review of current data on viral apoptosis suppression and oncogenesis.

Main Results:

  • Oncogenic viruses manipulate both extrinsic and intrinsic apoptosis pathways.
  • Viruses inhibit proapoptotic proteins and signaling pathways, promoting carcinogenesis.
  • Impaired immune surveillance contributes to uncontrolled viral replication and host cell proliferation.

Conclusions:

  • Viral suppression of apoptosis is a key mechanism in cancer development.
  • Understanding these mechanisms offers insights into viral oncogenesis.

Related Concept Videos

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...
6.2K
Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
37.6K
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...
5.8K
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
7.6K
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
7.4K