We can acquire new HPV types...re-infection with a new HPV type is possible with a new sex partner...also the virus can reactivate years after the initial infection. The body can build cell immunity to an acquired HPV type...but it may not...years later showing abnormal cell changes...
There is no cure for the virus...so tell future sex partners of your past HPV infection....
Maybe this will help
The virus takes up residence in our cells and alter the properties of that cell…the cell is transformed…the virus can stay in a sleeping state or does not replicated due to the cell me immunity.
Papillomaviruses are a diverse group of DNA-based viruses that infect the skin and mucous membranes of humans and a variety of animals (replicating exclusively in keratinocytes).
In an article published in the Proceedings of the National Academy of Sciences in March, the research team reports that a viral replication protein known as E2 binds the circular viral DNA to cell structures called spindle fibers that are present in a cell when it divides, a process known as mitosis. In mitosis, a single cell divides in two, creating two genetically identical daughter cells. By latching onto the spindle fibers of the cell as it divides, HPV DNA also divides and replicates itself in each of the new daughter cells where it can continue to replicate and persist indefinitely.
“In effect, HPV is able to mimic our own chromosomes, behaving as a sort of ‘mini-chromosome’, independently replicating and keeping pace as the cellular chromosomes replicate and the cell divides,” says Tom Broker, PhD, professor of biochemistry and molecular genetics and co-author of the paper. “This allows the virus to remain in our bodies indefinitely, with the potential of causing serious disease years, even decades, after first exposure.
www.IPVSoc.org
Following infection, HPV enters a period of quiescence that lasts about 2-12 months. Most HPV infections resolve without symptoms (subclinical) at this stage, presumably due to the emergence of the host’s cell-mediated immune response beginning approximately 3 months after infection (Figure 17). This immune response either eradicates the virus or suppresses it to non-detectable levels. Therefore, it is not yet known whether an HPV infection that appears to have cleared clinically is really eradicated or simply remains below the sensitivity level for detection with current molecular techniques.
Some HPV infections are thought to be suppressed and their genomes maintained in a long-term latent state (i.e., subclinical infection with a very small group of cells presumably maintaining infection at low DNA copy numbers). Support for a latent state for HPV infection comes from the observation that in some women genital warts can resolve spontaneously only to recur (i.e., reactivate) during pregnancy or when the immune system becomes compromised (e.g., HIV infection). It is not yet clear how commonly latency occurs in immunocompetent hosts, its ultimate duration, the circumstances and mechanisms that trigger re-emergence of HPV into a detectable state, whether latent HPV infection is ultimately eliminated in most individuals, or whether latent infection can persist, possibly leading to cervical cancer.
http://www.merckmedicus.com/pp/us/hcp/diseasemodules/hpvd/natural-history.jsp
Mechanism of genomic instability in cells infected with the high-risk human papillomaviruses.
Kadaja M, Isok-Paas H, Laos T, Ustav E, Ustav M.
Institute of Molecular and Cell Biology, University of Tartu, Tartu, Estonia.
In HPV-related cancers, the "high-risk" human papillomaviruses (HPVs) are frequently found integrated into the cellular genome. The integrated subgenomic HPV fragments express viral oncoproteins and carry an origin of DNA replication that is capable of initiating bidirectional DNA re-replication in the presence of HPV replication proteins E1 and E2, which ultimately leads to rearrangements within the locus of the integrated viral DNA. The current study indicates that the E1- and E2-dependent DNA replication from the integrated HPV origin follows the "onion skin"-type replication mode and generates a heterogeneous population of replication intermediates. These include linear, branched, open circular, and supercoiled plasmids, as identified by two-dimensional neutral-neutral gel-electrophoresis. We used immunofluorescence analysis to show that the DNA repair/recombination centers are assembled at the sites of the integrated HPV replication. These centers recruit viral and cellular replication proteins, the MRE complex, Ku70/80, ATM, Chk2, and, to some extent, ATRIP and Chk1 (S317). In addition, the synthesis of histone gammaH2AX, which is a hallmark of DNA double strand breaks, is induced, and Chk2 is activated by phosphorylation in the HPV-replicating cells. These changes suggest that the integrated HPV replication intermediates are processed by the activated cellular DNA repair/recombina