Cottontail rabbit papillomavirus
Papilloma
Papillomavirus Infections
Rabbits
Tumor Virus Infections
Oncogene Proteins, Viral
Papillomaviridae
Papillomavirus Vaccines
Viral Vaccines
Viral Structural Proteins
Vaccines, DNA
Lagomorpha
Base Sequence
Molecular Sequence Data
Human papillomavirus 16
Hares
Papillomavirus E7 Proteins
Protection of rabbits from viral challenge by gene gun-based intracutaneous vaccination with a combination of cottontail rabbit papillomavirus E1, E2, E6, and E7 genes. (1/83)
In this study, cottontail rabbit papillomavirus infection of domestic rabbits was used as an animal model to develop papillomavirus early gene-based vaccines. Groups of rabbits were intracutaneously vaccinated with single papillomavirus early genes E1, E2, E6, and E7 or with a combination of these four genes. Only a fraction of rabbits were protected from subsequent viral challenge when vaccinated with the E1 or E6 gene. Viral tumor growth in those rabbits vaccinated with the E1 or E2 gene was suppressed compared to that in controls. In contrast, seven of nine rabbits vaccinated with the combination of the E1, E2, E6, and E7 genes were completely protected against viral challenge. These data indicated that intracutaneous genetic vaccination with the combination of the E1, E2, E6, and E7 genes can be an effective strategy for immunoprophylaxis of papillomavirus infection. (+info)Induction of E6/E7 expression in cottontail rabbit papillomavirus latency following UV activation. (2/83)
Latent human papillomavirus (HPV) infections are widespread in the genital and respiratory tracts and are a source of recurrent disease. This study used a cottontail rabbit papillomavirus (CRPV) model to determine the presence of E1, E6, and E7 transcripts in latent infection and to determine the temporal change in transcripts following UV activation. We found E1 transcripts in all latently infected sites but no detectable E6 and E7 transcripts, consistent with our earlier studies of HPV6/11 latency. These results suggest that this transcription pattern is broadly characteristic of latent papillomavirus infections. E6/E7 transcripts were detectable within 1 week of irradiation, with maximal induction (approximately 40% of sites) at 2 weeks postirradiation. Papillomas were induced in approximately 26% of irradiated sites after a 3- to 5-week lag. Sites that did not form papillomas by 3 months after irradiation were CRPV DNA positive but E6/E7 RNA negative. Thus, only a subset of latent infections can be induced to express E6/E7 transcripts and form papillomas. We propose that CRPV can be used to study the molecular processes regulating papillomavirus activation. (+info)Rabbit oral papillomavirus complete genome sequence and immunity following genital infection. (3/83)
Rabbit oral papillomavirus (ROPV) infects mucosal tissues of domestic rabbits. The viral genomic sequence has been determined and the most related papillomavirus type was the cutaneous cottontail rabbit papillomavirus (CRPV). Homologies between the open reading frames (ORFs) of ROPV and CRPV, however, ranged from 68% amino acid identity for L1 to only 23% identity for E4. Shared features unique to the two rabbit viruses included a large E6 ORF and a small E8 ORF that overlapped the E6 ORF. Serological responses to ROPV L1 viruslike particles (VLPs) were detected in rabbits infected at either the genital or oral mucosa with ROPV. The antibody response was specific to intact ROPV L1 VLP antigen, was first detected at the time of late regression, and persisted at high levels for several months after complete regression. Both oral and genital lesions regressed spontaneously, accompanied by a heavy infiltrate of lymphocytes. ROPV infection of rabbit genital mucosa is a useful model to study host immunological responses to genital papillomavirus infections. (+info)Granulocyte-macrophage colony-stimulating factor priming plus papillomavirus E6 DNA vaccination: effects on papilloma formation and regression in the cottontail rabbit papillomavirus--rabbit model. (4/83)
A cottontail rabbit papillomavirus (CRPV) E6 DNA vaccine that induces significant protection against CRPV challenge was used in a superior vaccination regimen in which the cutaneous sites of vaccination were primed with an expression vector encoding granulocyte-macrophage colony-stimulating factor (GM-CSF), a cytokine that induces differentiation and local recruitment of professional antigen-presenting cells. This treatment induced a massive influx of major histocompatibility complex class II-positive cells. In a vaccination-challenge experiment, rabbit groups were treated by E6 DNA vaccination, GM-CSF DNA inoculation, or a combination of both treatments. After two immunizations, rabbits were challenged with CRPV at low, moderate, and high stringencies and monitored for papilloma formation. As expected, all clinical outcomes were monotonically related to the stringency of the viral challenge. The results demonstrate that GM-CSF priming greatly augmented the effects of CRPV E6 vaccination. First, challenge sites in control rabbits (at the moderate challenge stringency) had a 0% probability of remaining disease free, versus a 50% probability in E6-vaccinated rabbits, and whereas GM-CSF alone had no effect, the interaction between GM-CSF priming and E6 vaccination increased disease-free survival to 67%. Second, the incubation period before papilloma onset was lengthened by E6 DNA vaccination alone or to some extent by GM-CSF DNA inoculation alone, and the combination of treatments induced additive effects. Third, the rate of papilloma growth was reduced by E6 vaccination and, to a lesser extent, by GM-CSF treatment. In addition, the interaction between the E6 and GM-CSF treatments was synergistic and yielded more than a 99% reduction in papilloma volume. Finally, regression occurred among the papillomas that formed in rabbits treated with the E6 vaccine and/or with GM-CSF, with the highest regression frequency occurring in rabbits that received the combination treatment. (+info)DNA vaccination prevents and/or delays carcinoma development of papillomavirus-induced skin papillomas on rabbits. (5/83)
Malignant progression is a life-threatening consequence of human papillomavirus-associated lesions. In this study, we tested the efficacy of papillomavirus early-gene-based vaccines for prevention of carcinoma development of papillomavirus-induced skin papillomas on rabbits. Rabbit skin papillomas were initiated by infection with cottontail rabbit papillomavirus (CRPV). The papillomas were allowed to grow for 3 months without any treatment intervention. Rabbits were then immunized by gene gun-mediated intracutaneous administration of four DNA plasmids encoding CRPV E1, E2, E6, and E7 genes, respectively. All eight control rabbits receiving vector alone developed invasive carcinoma within 8 to 13 months. In contrast, only two of eight vaccinated rabbits developed carcinoma at 12 and 15 months, respectively. Papilloma growth was suppressed in the majority of vaccinated rabbits but not completely eradicated. These results indicate that gene gun-mediated immunization with papillomavirus early genes may be a promising strategy for prevention of malignant progression of human papillomavirus-associated lesions in humans. (+info)High and low levels of cottontail rabbit papillomavirus E2 protein generate opposite effects on gene expression. (6/83)
The papillomavirus E2 protein plays an important role in viral transcriptional regulation and replication. We chose to study the cottontail rabbit papillomavirus (CRPV) E2 protein as a transcriptional regulator because of the availability of an animal model for papilloma formation, which may be relevant for human papillomavirus (HPV) infection and replication. We studied the effect of expression levels of E2 on the long control region, which contains transcriptional promoter and enhancer elements, and synthetic E2-dependent artificial promoters in which the E2 was the dominant factor in the transcriptional activation. These experiments indicated that high levels of E2 were inhibitory and low levels were stimulatory for transactivation. In addition, we showed that the complex formed between CRPV E2 and the cognate binding site was less stable than the complex formed between HPV E2 and the same cognate binding site. Furthermore, we showed that CRPV E2 binding to its transcriptional regulatory sequence was stabilized by other proteins such as E1, which produced increments in transcriptional activation of E2-dependent genes. The data may be used to define conditions in which the rabbit model can be used for the screening of drugs which are inhibitory to the HPV and CRPV replication and gene expression. (+info)Variation in the nucleotide sequence of cottontail rabbit papillomavirus a and b subtypes affects wart regression and malignant transformation and level of viral replication in domestic rabbits. (7/83)
We previously reported the partial characterization of two cottontail rabbit papillomavirus (CRPV) subtypes with strikingly divergent E6 and E7 oncoproteins. We report now the complete nucleotide sequences of these subtypes, referred to as CRPVa4 (7,868 nucleotides) and CRPVb (7,867 nucleotides). The CRPVa4 and CRPVb genomes differed at 238 (3%) nucleotide positions, whereas CRPVa4 and the prototype CRPV differed by only 5 nucleotides. The most variable region (7% nucleotide divergence) included the long regulatory region (LRR) and the E6 and E7 genes. A mutation in the stop codon resulted in an 8-amino-acid-longer CRPVb E4 protein, and a nucleotide deletion reduced the coding capacity of the E5 gene from 101 to 25 amino acids. In domestic rabbits homozygous for a specific haplotype of the DRA and DQA genes of the major histocompatibility complex, warts induced by CRPVb DNA or a chimeric genome containing the CRPVb LRR/E6/E7 region showed an early regression, whereas warts induced by CRPVa4 or a chimeric genome containing the CRPVa4 LRR/E6/E7 region persisted and evolved into carcinomas. In contrast, most CRPVa, CRPVb, and chimeric CRPV DNA-induced warts showed no early regression in rabbits homozygous for another DRA-DQA haplotype. Little, if any, viral replication is usually observed in domestic rabbit warts. When warts induced by CRPVa and CRPVb virions and DNA were compared, the number of cells positive for viral DNA or capsid antigens was found to be greater by 1 order of magnitude for specimens induced by CRPVb. Thus, both sequence variation in the LRR/E6/E7 region and the genetic constitution of the host influence the expression of the oncogenic potential of CRPV. Furthermore, intratype variation may overcome to some extent the host restriction of CRPV replication in domestic rabbits. (+info)Combination treatment with intralesional cidofovir and viral-DNA vaccination cures large cottontail rabbit papillomavirus-induced papillomas and reduces recurrences. (8/83)
We used the cottontail rabbit papillomavirus (CRPV) New Zealand White rabbit model to test a combination treatment of large established papillomas with intralesional cidofovir and DNA vaccination to cure sites and reduce recurrences. Intralesional 1% (wt/vol) (0.036 M) cidofovir treatment of rabbit papillomas led to elimination, or "cure," of the papillomas over a 6- to 8-week treatment period (N. D. Christenson, M. D. Pickel, L. R. Budgeon, and J. W. Kreider, Antivir. Res. 48:131-142, 2000). However, recurrences at periods from 1 to 8 weeks after treatment cessation were observed at approximately 50% of cured sites. DNA vaccinations with CRPV E1, E2, E6, and E7 were initiated either after or at the time of intralesional treatments, and the recurrence rates were observed. When DNA vaccinations were started after intralesional cures, recurrence rates were similar to those of vector-vaccinated rabbits. A small proportion of recurrent sites subsequently regressed (4 out of 10, or 40%) in the vaccinated group versus no regression of recurrences in the vector-immunized group (0 out of 19, or 0%), indicating partial effectiveness. In contrast, when DNA vaccinations were conducted during intralesional treatments, a significant reduction of recurrences (from 10 out of 19, or 53%, of sites in vector-immunized rabbits to 3 out of 20, or 15%, of sites in viral-DNA-immunized rabbits) was observed. DNA vaccination without intralesional treatments had a minimal effect on preexisting papillomas. These data indicated that treatment with a combination of antiviral compounds and specific immune stimulation may lead to long-term cures of lesions without the ensuing problem of papilloma recurrence. (+info)Papillomas can occur anywhere on the body, but they are most commonly found on the face, neck, and scalp. They may appear as small bumps or growths that look like a wart. In some cases, papillomas may be associated with human papillomavirus (HPV) infection.
Papillomas are typically diagnosed through a physical examination of the affected area. In some cases, a biopsy may be performed to confirm the diagnosis and rule out other potential causes. Treatment for papillomas usually involves removal of the growth through a minor surgical procedure or cryotherapy (freezing).
Papillomas are not cancerous and do not typically pose any long-term health risks. However, they may be unsightly and can cause psychological distress for some people. In these cases, treatment may be sought for cosmetic reasons. It is important to note that papillomas should not be confused with squamous cell carcinoma, a type of skin cancer that can resemble a papilloma in appearance but has the potential to be more aggressive and harmful.
Papillomavirus infections can be classified into two main categories: low-risk and high-risk. Low-risk papillomavirus infections typically cause benign growths such as common warts, which are usually harmless and resolve on their own over time. High-risk papillomavirus infections, on the other hand, can lead to serious health problems such as cancer, particularly cervical cancer in women and anal cancer in both men and women.
The most common form of papillomavirus infection is genital warts, which are caused by human papillomavirus (HPV). HPV is the most common sexually transmitted virus and affects both men and women. It is estimated that up to 80% of people will be infected with HPV at some point in their lifetime, but most will not develop any symptoms or complications.
Other forms of papillomavirus infections include plantar warts, which are common on the soles of the feet and palms of the hands, and flat warts, which are small, rough growths that can appear anywhere on the body.
Papillomavirus infections can be diagnosed through a variety of methods, including visual inspection, biopsy, and molecular tests such as PCR (polymerase chain reaction). Treatment options vary depending on the type and location of the infection, but may include cryotherapy (freezing), surgical removal, or topical medications. Vaccines are also available to protect against certain types of papillomaviruses, particularly HPV.
Overall, papillomavirus infections are a common and diverse group of conditions that can have significant health implications if left untreated or if they progress to more severe forms. Proper diagnosis and treatment are important for managing these infections and preventing long-term complications.
There are several different types of tumor viruses, including:
1. Human papillomavirus (HPV): This virus is responsible for causing cervical cancer and other types of cancer, such as anal, vulvar, vaginal, and penile cancer.
2. Hepatitis B virus (HBV): This virus can cause liver cancer, known as hepatocellular carcinoma (HCC).
3. Human immunodeficiency virus (HIV): This virus can increase the risk of developing certain types of cancer, such as Kaposi's sarcoma and lymphoma.
4. Epstein-Barr virus (EBV): This virus has been linked to the development of Burkitt lymphoma and Hodgkin's lymphoma.
5. Merkel cell polyomavirus (MCPyV): This virus is responsible for causing Merkel cell carcinoma, a rare type of skin cancer.
6. Human T-lymphotropic virus (HTLV-1): This virus has been linked to the development of adult T-cell leukemia/lymphoma (ATLL).
Tumor virus infections can be diagnosed through a variety of methods, including blood tests, imaging studies, and biopsies. Treatment for these infections often involves antiviral medications, chemotherapy, and surgery. In some cases, tumors may also be removed through radiation therapy.
It's important to note that not all tumors or cancers are caused by viruses, and that many other factors, such as genetics and environmental exposures, can also play a role in the development of cancer. However, for those tumor virus infections that are caused by a specific virus, early diagnosis and treatment can improve outcomes and reduce the risk of complications.
Overall, tumor virus infections are a complex and diverse group of conditions, and further research is needed to better understand their causes and develop effective treatments.
There are several types of warts, including:
* Common warts: These are the most common type of wart and appear as rough, bumped growths on the skin.
* Flat warts: These are smaller and smoother than common warts and can appear on the face, neck, or arms.
* Plantar warts: These are found on the soles of the feet and can be painful.
* Genital warts: These are a type of HPV infection that appears in the genital area and can be spread through sexual contact.
Warts are usually diagnosed by a healthcare provider based on their appearance. In some cases, a biopsy may be performed to confirm the diagnosis.
Treatment for warts depends on the type and location of the growth, as well as the patient's overall health. Some common treatment options include:
* Cryotherapy: This involves freezing the wart with liquid nitrogen to kill the infected cells.
* Cantharidin: A blistering agent made from the secretions of the blister beetle, it is applied to the wart and causes a painless blister to form under the wart, which eventually falls off.
* Salicylic acid: A common ingredient in over-the-counter wart removers, it works by dissolving the keratin protein that makes up the wart.
* Surgical removal: In some cases, surgical removal of the wart may be necessary if other treatments have been unsuccessful.
* Immunotherapy: This is a newer treatment for warts that uses a patient's own immune system to fight off the HPV infection. It involves applying a solution to the wart that stimulates the immune system and causes the wart to fall off.
It is important to note that while warts are usually harmless, they can be a sign of a weakened immune system, so it is important to consult with a healthcare professional if you have any concerns. Additionally, it's important to avoid using over-the-counter treatments for long periods of time or on multiple areas of the body, as they can cause skin irritation and scarring.
Shope papilloma virus
Bettie Steinberg
Kathrin Jansen
Papillomaviridae
Oncovirus
List of MeSH codes (B04)
Gérard Orth
Francis Peyton Rous
Jackalope
Richard Shope
Biomarkers Search
Papillomavirus can be transmitted through the blood and produce infections in blood recipients: Evidence from two animal models...
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Tracking vaginal, anal and oral infection in a mouse papillomavirus infection model | Microbiology Society
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Etymologia: Papillomavirus - Volume 20, Number 5-May 2014 - Emerging Infectious Diseases journal - CDC
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Zhi-Ming Zheng, M.D., Ph.D. | Principal Investigators | NIH Intramural Research Program
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Mark A. Vecchiotti, MD | Tufts Medical Center | Tufts Medical Center
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INFECTIOUS PAPILLOMATOSIS OF RABBITS : WITH A NOTE ON THE HISTOPATHOLOGY - PubMed
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Science Clips - Volume 9, Issue 40, October 10, 2017
c33c
Function of cottontail rabbit papillo2
Protein of bovine papillomavirus type2
Shope2
Tumor2
- From the Latin papillo- ("nipple") + oma ("tumor"), papillomaviruses are nonenveloped DNA viruses that induce exophytic lesions of the skin and mucous membranes. (cdc.gov)
- The E10 ORF was named in July 2016, based on suggestions from senior members of the papillomavirus community at the DNA Tumor Virus Conference in Montreal. (nih.gov)
Infection5
- We report a proof-of-principle study to monitor the viral DNA copy number using a newly established mouse papillomavirus (MmuPV1) mucosal infection model. (microbiologyresearch.org)
- To our knowledge, our study is the first in vivo study to sequentially monitor papillomavirus infection from mucosal anal, oral and vaginal tracts in a preclinical model. (microbiologyresearch.org)
- 1) Papillomavirus infection and viral and host gene expression. (nih.gov)
- Human papillomavirus type 16 (HPV16) or 18 (HPV18) infection, acquired primarily via sexual transmission, is widely recognized as a leading cause of cervical and anal cancer as well as oropharyngeal cancer. (nih.gov)
- Mouse papillomavirus type 1 and cotton-tail rabbit papillomavirus infection models are two gold-standard preclinical animal models for studying HPV-associated infections and tumors. (nih.gov)
Viral Replication2
Cervical1
- In 1975, Harald zur Hausen published the hypothesis that the human papillomavirus played a role in the etiology of cervical cancer, work for which he was awarded the Nobel Prize in Physiology or Medicine in 2008. (cdc.gov)
Genome3
- 17. The Cellular DNA Helicase ChlR1 Regulates Chromatin and Nuclear Matrix Attachment of the Human Papillomavirus 16 E2 Protein and High-Copy-Number Viral Genome Establishment. (nih.gov)
- 20. Brd4 is required for e2-mediated transcriptional activation but not genome partitioning of all papillomaviruses. (nih.gov)
- The nucleotide sequence and genome organization of bovine papillomavirus type 4. (nih.gov)
Gene expression1
- 10. High and low levels of cottontail rabbit papillomavirus E2 protein generate opposite effects on gene expression. (nih.gov)
Viruses1
- At this point, E10 ORFs are only annotated in PaVE for Xi and Kappa papillomaviruses, since there is published evidence for the function of these proteins in these viruses. (nih.gov)
Transcription3
- 8. Phosphorylation of the Bovine Papillomavirus E2 Protein on Tyrosine Regulates Its Transcription and Replication Functions. (nih.gov)
- 15. Control of human papillomavirus type 11 origin of replication by the E2 family of transcription regulatory proteins. (nih.gov)
- 19. Identification of the E9/E2C cDNA and functional characterization of the gene product reveal a new repressor of transcription and replication in cottontail rabbit papillomavirus. (nih.gov)
Human12
- 2. Mitogen-activated protein kinases activate the nuclear localization sequence of human papillomavirus type 11 E1 DNA helicase to promote efficient nuclear import. (nih.gov)
- 3. Human Papillomavirus Replication Regulation by Acetylation of a Conserved Lysine in the E2 Protein. (nih.gov)
- 4. Inhibition of human papillomavirus DNA replication by small molecule antagonists of the E1-E2 protein interaction. (nih.gov)
- 5. Human papillomavirus type 31 replication modes during the early phases of the viral life cycle depend on transcriptional and posttranscriptional regulation of E1 and E2 expression. (nih.gov)
- 9. Cyclin/CDK regulates the nucleocytoplasmic localization of the human papillomavirus E1 DNA helicase. (nih.gov)
- 12. Evidence supporting a role for TopBP1 and Brd4 in the initiation but not continuation of human papillomavirus 16 E1/E2-mediated DNA replication. (nih.gov)
- 13. The hinge of the human papillomavirus type 11 E2 protein contains major determinants for nuclear localization and nuclear matrix association. (nih.gov)
- 18. Recruitment of Brd4 to the human papillomavirus type 16 DNA replication complex is essential for replication of viral DNA. (nih.gov)
- Anorectal human papillomavirus: current concepts. (microbiologyresearch.org)
- The prevalence of human papillomavirus in colorectal adenomas and adenocarcinomas: a systematic review and meta-analysis. (microbiologyresearch.org)
- Human papillomavirus in the HIV-infected host: epidemiology and pathogenesis in the antiretroviral era. (microbiologyresearch.org)
- Comparative analysis of the human type 1a and bovine type 1 papillomavirus genomes. (nih.gov)
Type2
Mouse1
- 5. Photodynamic therapy of cottontail rabbit papillomavirus-induced papillomas in a severe combined immunodeficient mouse xenograft system. (tuftsmedicalcenter.org)
Entry1
- 7. Acetylation of E2 by P300 Mediates Topoisomerase Entry at the Papillomavirus Replicon. (nih.gov)
Open1
- The B subgroup bovine papillomaviruses lack an identifiable E6 open reading frame. (nih.gov)
Essential1
- Cottontail rabbit papillomavirus E8 protein is essential for wart formation and provides new insights into viral pathogenesis. (nih.gov)
Wild cottontail rabbits2
Induces2
- 2. Papillomavirus E2 protein induces expression of the matrix metalloproteinase-9 via the extracellular signal-regulated kinase/activator protein-1 signaling pathway. (nih.gov)
- 2002. Intracutaneous DNA vaccination with the E8 gene of cottontail rabbit papillomavirus induces protective immunity against virus challenge in rabbits. (nih.gov)
PAPILLOMATOSIS OF RABBITS1
- Infectious papillomatosis of rabbits. (cdc.gov)
Lesions3
- Both invasive cervical cancers and precursor lesions have been firmly associated with the presence of human papillomavirus (HPV) DNA. (nih.gov)
- From the Latin papillo- ("nipple") + oma ("tumor"), papillomaviruses are nonenveloped DNA viruses that induce exophytic lesions of the skin and mucous membranes. (cdc.gov)
- A genus of DNA viruses in the family PAPILLOMAVIRIDAE , causing cutaneous and mucosal lesions in rabbits. (nih.gov)
Bovine5
- Cell transformation by the E5/E8 protein of bovine papillomavirus type 4. (nih.gov)
- Comparative analysis of the human type 1a and bovine type 1 papillomavirus genomes. (nih.gov)
- The B subgroup bovine papillomaviruses lack an identifiable E6 open reading frame. (nih.gov)
- The nucleotide sequence and genome organization of bovine papillomavirus type 4. (nih.gov)
- Analysis of the transforming functions of bovine papillomavirus type 4. (nih.gov)
Viruses1
- At this point, E10 ORFs are only annotated in PaVE for Xi and Kappa papillomaviruses, since there is published evidence for the function of these proteins in these viruses. (nih.gov)
Papillomata2
- Rabbits carrying experimentally produced papillomata are partially or completely immune to reinfection and, furthermore, their sera partially or completely neutralize the causative virus. (nih.gov)
- The disease is transmissible in series through wild rabbits and virus of wild rabbit origin is readily transmissible to domestic rabbits, producing in this species papillomata identical in appearance with those found in wild rabbits. (nih.gov)
Cervical cancer2
- 11. Triggering of death receptor apoptotic signaling by human papillomavirus 16 E2 protein in cervical cancer cell lines is mediated by interaction with c-FLIP. (nih.gov)
- In 1975, Harald zur Hausen published the hypothesis that the human papillomavirus played a role in the etiology of cervical cancer, work for which he was awarded the Nobel Prize in Physiology or Medicine in 2008. (cdc.gov)
Gene1
- E10 is now designated as an ORF that either overprints the E6 ORF, or is encoded in this region (in the absence of an E6 gene) in certain papillomaviruses. (nih.gov)
Protein4
- 3. AP-1 and ERK1 but not p38 nor JNK is required for CRPV early protein 2-dependent MMP-9 promoter activation in rabbit epithelial cells. (nih.gov)
- Control of viral replication and transcription by the papillomavirus E8^E2 protein. (nih.gov)
- 1996. Transforming properties of the cottontail rabbit papillomavirus oncoproteins Le6 and SE6 and of the E8 protein. (nih.gov)
- Cottontail rabbit papillomavirus E8 protein is essential for wart formation and provides new insights into viral pathogenesis. (nih.gov)
Infectious1
- The virus of infectious papillomatosis is not related immunologically to either the virus of infectious fibroma or to that of infectious myxoma of rabbits. (nih.gov)
Virus1
- The E10 ORF was named in July 2016, based on suggestions from senior members of the papillomavirus community at the DNA Tumor Virus Conference in Montreal. (nih.gov)