Causes, Viruses: HPV
In this section learn how viruses contribute to cancer development.
Viruses are infectious agents that can replicate only within the cells of other living organisms. Humans are affected by a variety of viruses. Some cause minor illnesses like the common cold; others can lead to more serious conditions like influenza and AIDs. Click on the buttons to the left to find out more about the human papillomavirus (HPV) and its link to cervical cancer. HPV Human papillomavirus (HPV) is a large family of viruses best known for causing warts. Some HPV types have been linked to cervical cancer. Click the forward arrow or the numbers below to find out more about the human papillomavirus (HPV). Bettie Steinberg, Ph.D., talks about HPV and its prevalence among the population. â€œO.K. HPVs are a family of related viruses. They're in a group called the small DNA tumor viruses, which means they have DNA inside the virus and they can cause tumors in either their natural host or another organism. The HPVs are human papilloma viruses. There are more than a hundred different types and they are extremely common. Some of the types cause skin warts, or plantar warts. Other types infect the mucus membranes and they cause things like genital warts and genital tract infections. They are extremely common. Everybody has these viruses. We have them in our skin and and we have them in our mucus membranes. They live with us. And the estimate is that at least 70% of women will have an HPV infection of the genital tract, primarily the cervix at some time, during their life.â€ Denise Galloway, Ph.D., talks about HPV and its link to cervical cancer and how HPV infection affects normal cellular processes. â€œThere are many HPVs that infect the genital tract and a set of those cause benign genital warts but another set is able to cause lesions that will go on and progress to cervical or other anal-genital cancers. I think the link is very firmly established. There are, have been many large international studies that have looked for the presence of HPV in cervical cancers and found that nearly 100% of them are positive for the viral DNA. I think the mechanisms are pretty well understood. When HPV infects the genital epithelium, it causes those cells to proliferate when they normally would not. It also causes the normal checkpoints that would prevent the cell from replicating if there is DNA damage or damage to the chromosomes, it inactivates those checkpoints so that the cells that receive damage can still continue to replicate.â€ â€œViruses don't want to cause cancer, they just want to make more virus. But this virus has really none of its own machinery for replication. And so the only way it can replicate itself is to be in a cell that's replicating, so that it can use the cellular replication machinery. So it gets into a cell and in order to make its viral proteins, it needs to push that cell into cellular replication. And it does so with the expense of the cell's normal control. Normally the outcome is that you get more virus. So cancer is actually a very rare outcome for HPV infection.â€ HPV and cell cycle Cell growth and replication are tightly regulated processes. Viral proteins disrupt this growth cycle by interacting and binding with host proteins. Click the forward arrow or the numbers below to find out more about the cell cycle and how human papillomavirus (HPV) viral proteins interact with cellular proteins. Ed Harlow, Ph.D. is the Chair of the Department of Biological Chemistry and Molecular Pharmacology at Harvard Medical School. His research focuses on developing new ways to analyze and identify genes involved in key regulatory pathways in the cell. â€œOver the years, we have learned that the cell cycle can easily be divided in a couple of major decision points or action points where cells specifically do a series of tasks that need to go through. The two major ones that are the replication of the DNA, the actual chromosomes being replicated and duplicated into an exact copy something called DNA synthesis, is highlighted as the S-phase in the eukaryotic cell cycle world. And the other big part is mitosis, when the cell actually divides and that's called M-phase. And those two phases are kind of the big action points in everything big happens in the cell division cycle. However, there are obviously very tightly controlled, you obviously don't want to do these at inappropriate times or without the right type of regulation, so there actually are control points that happen just before the action of DNA synthesis or before M-phase and we call those in our world gap phases or G1 and G2. So it really does look like a cycle when you begin to think about it. It's a circle in which cells go from G1 to S, G2 to M, and back to G1 and they continue this cycle around. And at each point there are relatively complicated decision making points that a cell assesses whether it's a good idea to divide or not or go to the next stage.â€
dna tumor viruses, human papillomavirus hpv, human papilloma viruses, hpv types, hpv infection, skin warts, human papillomavirus, mucus membranes, plantar warts, genital warts, minor illnesses, living organisms, genital tract, cervical cancer, natural host, cellular processes, infectious agents, tract infections, cervix
- ID: 999
- Source: DNALC.IC
Professor Steinberg explains that HPVs are a family of related viruses, and they're small DNA tumor viruses that can cause tumors in either their natural host or another organism.
Professor Galloway explains that there are many HPVs that infect the genital tract and a set of those cause benign genital warts but another set is able to cause lesions that will go on and progress to cervical or other anal-genital cancers.
Professor Galloway explains that viruses don't want to cause cancer, they just want to make more virus.
Mike Wigler shows how all organisms share similar genes, called homologs.
Aflatoxin, a byproduct of molds, is a potent cancer-causing agent. Long-term exposure to aflatoxin has been linked to increased incidence of liver cancer.
David Baltimore and Howard Temin explain work on the Rous sarcoma virus.
Paul Berg's student, Janet Mertz, planned an experiment that would recombine DNA from a monkey virus with DNA from a bacterium that lives in the human gut. Berg describes colleague Bob Pollack's outrage at this.
Conventional cancer drugs are cellular poisons that block replication or some other aspect of cell growth. These drugs affect all cells – healthy or cancerous.
Mature virus particles released from host cell.
Renowned biologist and philosopher Robert Pollack reflects on his concern over the potential danger of Janet Mertz's experiment inserting a cancer-causing gene from a monkey virus into a bacterium that lives in humans.