SEARCH · PubMed Health

Results for “Human Papillomavirus Viruses”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

PubMedDate not supplied

Human immunodeficiency virus, human papillomavirus, and cervical intraepithelial neoplasia in Nairobi prostitutes.

To evaluate the impact of human immunodeficiency virus (HIV) on human papillomavirus (HPV) and cervical intraepithelial neoplasia (CIN), a study was conducted of 147 HIV-seropositive and 51 HIV-seronegative prostitutes in Nairobi, Kenya. Among the women infected with HIV, 10 (7%) had signs or symptoms of significant HIV-related disease, and the remaining 93% were asymptomatic. The prevalence of cervical HPV DNA was 37% among HIV-seropositive women and 24% in HIV-seronegative women (odds ratio [OR] 1.7, 95% confidence intervals [CI] 0.8, 3.6, after adjusting for potential confounding factors). Genital warts, cervical HPV DNA, and cytologic findings consistent with CIN were all significantly associated with younger age and fewer years of prostitution, but were unrelated or weakly related to number of sexual partners per week or frequency of condom use. In a subset of 63 women with evaluable Papanicolaou smears, CIN was found in 50% of the women with HPV but only in 8% of those without HPV (adjusted OR 7.2, 95% CI 1.6, 32.1, P = 0.006). However, CIN was unrelated to HIV seropositivity (prevalence of 26% among HIV-seropositive women and 24% in HIV-seronegative women). Among women with cervical HPV DNA, HIV infection was not associated with an increased prevalence of CIN (47% prevalence among women with HIV versus 57% prevalence among women without HIV). Thus, in this population of HIV-seropositive women, most of whom had CDC Stage II or III infection, there was no demonstration of an adverse impact of HIV on CIN.

Adult↗

PubMed1990

Epidemiology of sexually transmitted diseases: the global picture.

Sexually transmitted diseases (STD) are now the commonest group of notifiable infectious diseases in most countries, particularly in the age group of 15 to 50 years and in infants. Their control is important considering the high incidence of acute infections, complications and sequelae, their socioeconomic impact, and their role in increasing transmission of the human immunodeficiency virus (HIV). The worldwide incidence of major bacterial and viral STD is estimated at over 125 million cases yearly. STD are hyperendemic in many developing countries. In industrialized countries, the bacterial STD (syphilis, gonorrhoea, chancroid) declined from the peak during the Second World War till up to the late fifties, then increased during the sixties and early seventies, and they have been decreasing again from the late seventies till the present. In the industrialized world, diseases due to Chlamydia trachomatis, genital herpes virus, human papillomaviruses and human immunodeficiency virus are now more important than the classical bacterial ones; both groups remain major health problems in most developing countries. Infection rates are similar in both women and men, but women and infants bear the major burden of complications and serious sequelae. Infertility and ectopic pregnancies are often a consequence of pelvic inflammatory disease, and are preventable. Sexually transmitted diseases in pregnant women can result in prematurity, stillbirth and neonatal infections. In many areas 1-5% of newborns are at risk of gonococcal ophthalmia neonatorum, a blinding disease; congenital syphilis causes up to 25% of perinatal mortality. Genital and anal cancers (especially cervical cancer) are associated with viral sexually transmitted diseases (genital human papillomavirus and herpes virus infections). Urethral stricture and infertility are frequent sequelae in men.

Adolescent↗

PubMed1989

Transformation of human cells by oncogenic viruses supports permissiveness for parvovirus H-1 propagation.

Parvovirus H-1 has been shown to suppress spontaneous and chemically or virally induced tumorigenesis in hamsters. In human cell culture systems propagation of H-1 is restricted to transformed cells, which are killed by H-1 infection, in contrast to normal diploid cells, which are nonpermissive for H-1. By analyzing the permissiveness of a variety of human cells for H-1, it was determined that the majority of tested transformed or immortalized cells which were permissive for H-1 contained the DNA of oncogenic viruses (human papillomavirus, simian virus 40, adenovirus, hepatitis B virus, Epstein-Barr virus, and human T-cell lymphotropic virus type I). Of six transformed cell lines negative for persisting tumor virus DNA, only two were permissive for H-1, while two were semipermissive and two were nonpermissive. Thus, persistence and expression of tumor virus functions appears to promote full permissiveness for H-1 in human cells. However, neither expression of genes of specific viral genomes nor the transformed state of apparently virus-free cells alone was sufficient to render human cells permissive for H-1. Therefore, the effect of tumor virus functions on H-1 in transformed cells seems to be indirect, probably mediated by cellular factors which are induced or switched off during the transformation process. It appears that similar factors are induced or switched off by 5-azacytidine or calcium phosphate, both known inducers of cellular gene expression.

Animals↗

PubMed1992

Prevalence of Epstein-Barr virus and human papillomavirus in oral mucosa of HIV-infected patients.

Epstein-Barr virus (EBV) has been implicated in the genesis of oral hairy leukoplakia (OHL). Initially, OHL was also associated with human papillomavirus (HPV) as evidenced by staining with antiserum to papillomavirus common structural antigens and reports of two HPV-positive OHL as detected by in situ DNA hybridization. The aims of this study were to determine the prevalence of EBV and HPV DNA in OHL and normal oral mucosa and to explain the basis for the staining of OHL tissues with antibodies to papillomavirus common structural antigens. EBV DNA was detected by in situ hybridization in 47 of 47 cases of OHL from human immunodeficiency virus (HIV)-seropositive individuals and in 1 of 10 biopsies of clinically normal buccal mucosa from the same group of individuals. Twenty-five of 35 OHL specimens stained with antibody to papillomavirus common structural antigens. There was no staining of two EBV-containing lymphoblastoid lines, indicating that the staining with anti-papillomavirus antibody was not due to antigenic cross-reactivity with EBV antigens. HPV DNA was detected by polymerase chain reaction amplification in 10 of 18 OHL specimens and in 6 of 10 normal buccal mucosa specimens. Our results indicate that EBV and HPV are present frequently in OHL and that HPV can be found regularly in histologically normal mucosa.

Acquired Immunodeficiency Syndrome↗

PubMed1992

The 'other' sexually transmitted diseases. Chlamydial, herpes simplex virus, and human papillomavirus infections.

The incidence of sexually transmitted diseases continues to rise across the country. Because many cases are subclinical and asymptomatic, chlamydial, herpes simplex virus, and human papillomavirus (HPV) infections continue to spread at an alarming rate. These infections can lead to serious sequelae, such as pelvic inflammatory disease, infertility, and cervical dysplasia or carcinoma, so improved disease-control strategies are needed. Preventive efforts should include use of the latest diagnostic and therapeutic methods to uncover and eradicate subclinical chlamydial and HPV infections. In addition, notification of sexual partners should be encouraged. Education about prevention of sexually transmitted diseases should be incorporated into basic primary medical care for all sexually active patients.

Chlamydia Infections↗

PubMed2025

Oncoproteins E6/E7 of the human papillomavirus types 16 & 18 synergize in modulating oncogenes and tumor suppressor proteins in colorectal cancer.

OBJECTIVE: Our study presents a novel analysis of the oncogenes and tumor suppressor proteins directly modulated by E6/E7 of high-risk HPV types 16 and 18, in colorectal cancer (CRC). METHODS: HCT 116 (KRAS mutant) & HT-29 (TP53 mutant) cell models of CRC were transduced with E6/E7 of HPV16 and HPV18, individually and in combination. Further, we utilized a liquid chromatography mass spectrometry (LC-MS/MS) approach to analyze and compare the proteomes of both CRC cell models. RESULTS: We generated six stably transduced cell lines. Our data revealed a significantly higher, HPV-induced modulation of oncogenes and tumor suppressor proteins in the TP53 mutant model, as compared to the KRAS mutant model (p ≤ 0.01). Less than 1% of the genes were commonly modulated by HPV, between both models. We also report that HT-29 cells, expressing E6/E7 of both HPV types, significantly reduced the suppression of oncogenes as compared to cells expressing E6/E7 of either HPV types individually (p-value ≤0.00001). CONCLUSION: Our data imply that HPV coinfections leads to the sustenance of a pro-oncogenic environment in CRC. HPV modulates different oncogenes/tumor suppressor proteins in CRC of varying mutational backgrounds, thus highlighting the importance of personalized therapies for such diseases with mutational heterogeneity.

Humans↗

PubMed1991

The induction of cytotoxic T-lymphocyte precursor cells by recombinant vaccinia virus expressing human papillomavirus type 16 L1.

Expression of the major coat protein L1 of human papillomavirus type 16 by recombinant vaccinia viruses using a vaccinia late promoter and their use in generating antibodies have already been reported (Zhou et al., 1990). We have now constructed recombinant vaccinia viruses (VVs) which express the L1 protein from an early promoter with the intention of inducing cell-mediated immunity. This necessitated the removal of sequence motifs (TTTTTNT) from the L1 gene which would otherwise have caused transcription termination when expressed from a vaccinia virus early promoter. The nucleotide sequence was mutated to retain the correct amino acid sequence of the L1 protein. Full-length mRNA and L1 protein were generated in cells infected with the recombinant virus containing the mutant sequence, whereas the wild-type sequence generated only truncated mRNA and no detectable protein. Mice were immunized with VV expressing L1 from the mutant sequence and from the wild-type sequence in constructs with either early or late vaccinia virus promoters. Only the early promoter constructs were effective in priming cytotoxic T lymphocytes (CTL). Moreover the mutant sequence was significantly more effective than the wild-type sequence. The same L1 sequences, expressed from a vaccinia virus late promoter or coexpressed with MHC Class I molecules also expressed from a late promoter, produced high levels of L1 protein in both cases but nevertheless failed to elicit CTL activity. This is the first report of an HPV-specific CTL response and we have reaffirmed the importance of choosing the correct promoter and sequence expressed when using recombinant vaccinia viruses to induce cytotoxic T lymphocytes. These data are relevant for the design of vaccines to generate cell-mediated immunity against human papillomavirus infection.

Animals↗

PubMed1992

Human papillomavirus, human immunodeficiency virus, and cervical cancer: newly recognized associations?

There are now sufficient data to conclude that women infected with human immunodeficiency virus (HIV) have an increased risk of human papillomavirus (HPV) infection and preinvasive stages of cervical cancer. This association is not completely due to immunosuppression. It is likely that HPV pathogenesis is altered in HIV-infected women. Preinvasive cervical neoplasia likely occurs more frequently in HIV-infected women because of several factors, including immunosuppression, viral interactions, and alterations in viral pathogenesis. As new treatments prolong the life of HIV-infected individuals, we must continue to be aware of and reactive to an increasing number of opportunistic complications of HIV infection, such as HPV infection and associated diseases.

AIDS-Related Opportunistic Infections↗

PubMed1992

Herpes simplex virus and human papillomavirus sites correlate with chromosomal breakpoints in human cervical carcinoma.

The distribution of 1,912 breakpoints observed in a series of 148 cervical cancers was analyzed. Fifty bands were shown to be nonrandomly involved in chromosome structural rearrangements. One hundred thirty-three breaks were noted in bands known to contain a human papillomavirus integration site, and 454 breaks were noted in bands containing a herpes simplex virus breakage site. We suggest that herpes simplex viruses and, possibly, papillomaviruses play an important role in the carcinogenesis and/or development of cytogenetic abnormalities in cervical cancers.

Chromosome Aberrations↗

PubMed1985

A prospective study of association of herpes simplex virus and human papillomavirus infection with cervical neoplasia in women exposed to diethylstilbestrol in utero.

One thousand one hundred thirty-four women, enrolled in a prospective study of the development of cervical neoplasia in women exposed to diethylstilbestrol (DES) in utero, were examined at least once a year. Twenty-three women developed cervical intraepithelial neoplasia (CIN) of different degrees during the 7-year follow-up period and were matched with women who did not develop CIN during the study period. Serum samples were obtained at the time of entry into the study and at the time of diagnosis of neoplasia. In the control group, a second serum sample was obtained close to the time when CIN was diagnosed in the other group of women. The sera were studied for antibodies to both types of herpes simplex virus (HSV) by microneutralization assay and by a radioimmunoassay using, as antigens, glycoproteins VP123 for HSV type 1 and VP119 for HSV type 2. Women who developed CIN had, in the enrollment specimen which preceded the neoplasia, a higher rate of antibodies to HSV-1 than did the matched controls (22%), while the two groups did not differ in frequency of antibodies to HSV-2 (9%). Similar differences were observed in the sample drawn at the time of diagnosis of CIN. Women who later developed CIN and had, at the time of entry into the study, cervical epithelial changes associated with DES exposure, were infected with HSV-1 at a higher rate than women who remained free of neoplasia or women with CIN but without DES-associated cervical epithelial changes. Morphologic evidence of associated papillomavirus (HPV) infection was observed in 74% of CIN cases and no such observation was made in biopsy specimens taken prior to development of CIN. Morphologic evidence of HPV infection was found in a women of the control group having squamous metaplasia. HPV structural antigens were found in 3 of 10 CIN I and CIN II cases, and none in the CIN III specimens. The possible role of the HSV and HPV infection in the pathogenesis of cervical neoplasia is discussed.

Adolescent↗

PubMed1992

[Skin cancer and virus].

Human papillomaviruses (HPV) generally associated with benign skin and anogenital warts. Because several of skin cancers were found to contain HPV-DNA, it has been speculated that certain types of HPV could be specifically associated with cancers. Although HPV-DNAs are not isolated from most of skin cancers, they are often isolated from penile cancers, vulval cancers and anogenital Bowen's diseases. Patients with epidermodysplasia verruciformis start to suffer from disseminated incurable warts during their childhood, and some of these benign lesions often convert to skin cancer in adulthood. Although the disease is very rare, HPV may also play a role in malignant transformation in epidermodysplasia verruciformis. More than 60 types of HPVs distinguished by molecular hybridization techniques. The type of HPV determines the clinical picture of wart and natural fate of HPV-associated lesion. There are two groups of HPVs, which are benign types and malignant types. Viral DNA of malignant type of HPV transforms human keratinocytes in vitro, and the transforming activity has been mapped to the E6 and E7 genes.

Bowen's Disease↗

PubMed1989

Search for human papillomavirus, herpes simplex virus and c-myc oncogene in human genital tumors.

We tested grade III cervical intra-epithelial neoplasms (CIN III), genital invasive carcinomas and healthy genital tissues for the presence of a number of viral and cellular parameters, considered to be risk factors in genital oncogenesis. The results show that: (I) about 30% of genital tumors had homology to HSV-2 BglII N and/or BamHI E DNA fragments; (2) positivity to HSV-2-specific protein ICP10, encoded by sequences within the HSV-2 BamHI E DNA fragment, was detected in 29/55 neoplastic genital tissues but not in healthy genital tissues or tumors at other sites; (3) HPV-16 DNA was found in about 50% of tumor samples, but none of the positive tissues reacted to HPV capsid protein or to the protein encoded by the HPV-16 E6 ORF; (4) 6/8 tumor samples showing homology to HSV-2 DNA fragments also hybridized to HPV-16 DNA; (5) c-myc amplification was not detected in any of the analyzed samples, but tissues from 4 patients were positive for c-myc expression. None of the considered factors was present in all the analyzed samples; nevertheless, some tissues showed the simultaneous involvement of several parameters, suggesting that a number of risk factors may be involved in different steps of human genital oncogenesis.

Adenocarcinoma↗

PubMed1992

Dermatopathologic findings in patients infected with HIV.

Several inflammatory, infectious, and neoplastic conditions in HIV-infected patients are distinctive or require a biopsy for diagnosis. Some differ subtly from similar conditions seen in noninfected patients. The exanthem of acute HIV infection cannot be diagnosed specifically on biopsy as its histologic appearance is similar to that of other viral exanthemata. A condition that closely resembles seborrheic dermatitis occurs in HIV-infected patients. Plasma cells, necrotic keratinocytes, and leukocytoclasis may be present, in contrast to findings in sporadic seborrheic dermatitis. Psoriasis and Reiter's disease also occur in HIV-infected patients and can be specifically diagnosed as such. The category "psoriasiform dermatitis of AIDS" thus seems to include several distinct entities and not to be a single disease. Bacillary angiomatosis is a treatable infection caused by a rickettsialike organism similar to Rochalimaea quintana, the agent of trench fever. Cutaneous lesions are characterized by lobules of capillaries with protuberant endothelial cells, neutrophils and their debris, and purplish-staining clumps of organisms, which can be demonstrated with silver stains or electron microscopy. An unusual reaction to atypical mycobacterial infection, in which spindle-shaped macrophages are seen, resembles histoid leprosy. Viral skin diseases that may challenge the dermatopathologist include unusual verrucous reactions to chronic varicella-zoster infection and flat warts caused by the human papillomavirus associated with epidermodysplasia verruciformis. Keratinocytes with foamy basophilic cytoplasm may be a marker for one of these viruses, human papillomavirus type 5. Neoplastic complications of HIV disease include Kaposi's sarcoma and mycosis fungoides. The earliest lesions of the patch stage of Kaposi's sarcoma show a slightly increased number of cells with small ovoid nuclei around preexistent structures, accompanied, in some cases, by sparse infiltrates of lymphocytes and plasma cells. Staining with antisera to type IV collagen may highlight the vascular spaces in these early lesions. Later lesions that resemble hemangiomas may also prove challenging and require level sections to demonstrate the presence of spindle cells and eosinophilic globules. Although HIV is cytotoxic to helper T cells, neoplastic proliferations of them may be seen in HIV-infected patients. These cases of mycosis fungoides do not seem to differ from sporadically occurring ones and occur in patients who seem not to be infected by HTLV-I.

HIV Infections↗

PubMed1986

Genome organization and nucleotide sequence of human papillomavirus type 33, which is associated with cervical cancer.

The 7,909-nucleotide sequence of human papillomavirus type 33, which is associated with cervical cancer, has been determined and used to deduce the corresponding genome arrangement. Extensive sequence homologies and other genetic features are shared with the related oncogenic virus, human papillomavirus type 16, especially in the major reading frames. A surprising difference was found in the noncoding region of human papillomavirus type 33 as, unlike all other sequenced papillomaviruses, it contains a perfect 78-base pair tandem repeat.

Base Sequence↗

PubMed1992

Association of human immunodeficiency virus and anal human papillomavirus infection among homosexual men.

BACKGROUND: A previous study of men with proctitis, proctocolitis, or enteritis showed an association of anal human papillomavirus (HPV) infection with human immunodeficiency virus (HIV) infection. Because anorectal abnormalities may confound an observed association between anal HPV DNA and HIV seropositivity, the present study was undertaken among consecutive homosexual men seeking HIV serologic testing who were unselected for anorectal symptoms. METHODS: Consecutive homosexual men underwent a standardized interview, physical examination, and collection of specimens for HIV serologic testing and detection of anal HPV DNA. RESULTS: Anal HPV DNA was detected in eight (31%) of 26 HIV-seropositive men and in 10 (8%) of 119 HIV-seronegative men (odds ratio, 5.8; 95% confidence interval, 1.1 to 30.1, adjusted for history of sexually transmitted disease, current anorectal symptoms, and age). When men with anorectal symptoms were excluded from the analysis, anal HPV DNA was detected in 27% of seropositive men compared with 8% of seronegative men (odds ratio, 4.4; 95% confidence interval, 1.4 to 13.4). There was no difference between HIV-seropositive and HIV-seronegative men with respect to distribution of type of HPV DNA. Men with group II or III and group IV HIV disease were 4.1 and 10.9 times, respectively, more likely than HIV-seronegative men to have anal HPV DNA detected. CONCLUSIONS: Because HIV-seropositive men appear to be at increased risk for the detection of anal HPV DNA, the natural course of anal HPV infection should be compared among HIV-seropositive and HIV-seronegative homosexual men.

Anus Diseases↗

PubMed1990

Adenovirus infection induces amplification of persistent viral DNA sequences (simian virus 40, hepatitis B virus, bovine papillomavirus) in human and rodent cells.

Adenoviruses, types 2 and 12 induce amplification of SV40 DNA sequences in cells of the SV40-transformed human newborn kidney cell line, NB-E. Similarly, integrated hepatitis B virus DNA sequences in the human hepatoma cell line, PLC/*PRF/5, and bovine papillomavirus (BPV) DNA sequences in BPV-transformed mouse cells (ID13) are amplified by adenovirus infection. Thus, similar to herpes group or vaccinia viruses or DNA damaging agents, adenoviruses are able to mediate selective DNA amplification in addition to their reported mutagenic and chromosome damaging effects. The role of amplification of integrated viral DNA sequences in development and progression of specific tumors (e.g. hepatocellular carcinoma) remains to be determined.

Adenoviruses, Human↗

PubMed1988

Human papillomavirus and herpes simplex virus in vulvar squamous cell carcinoma in situ.

Human papillomavirus deoxyribonucleic acid were detected in tissue specimens from 38 to 46 patients (83%) with squamous cell carcinoma in situ of the vulva. Herpes simplex virus type 2--related antigen ICSP 34/35 was demonstrated in 23 of the lesions (50%), and antibodies to herpes simplex virus types 1 and 2 were found in 74% and 65% of the serum samples tested, respectively. Both human papillomavirus deoxyribonucleic acid and herpes simplex virus type 2 antigen were detected in 19 cases (41%). Correlation of human papillomavirus type to the ages of the patients revealed that types 16, 18, and 31 are most often seen in older patients, although the frequencies do not differ significantly. No relationship between the presence or absence of herpes simplex virus type 2--related antigen to age of the patient was observed.

Adult↗

PubMed1991

Vaginal cancer: the role of infectious and environmental factors.

Primary cancers of the vagina are rare. They comprise 1% to 2% of all gynecologic malignancies and occur predominantly in older women. The diagnosis of primary carcinoma of the vagina requires that the cervix and vulva be intact and that no clinical evidence of other primary tumors exist. Approximately 90% of all vaginal tumors are squamous cell in type on histologic examination. Adenocarcinoma, which is much less common (2% to 4%), is seen primarily in younger women with in utero exposure to diethylstilbestrol. In addition to exposure to diethylstilbestrol, other environmental factors have been associated with the development of vaginal tumors, including chronic irritation from pessaries, previous hysterectomy for benign disease, immunosuppression therapy, cervical irradiation, and endometriosis. Infectious causes seem to play an even more pernicious role in vaginal cancer. The two agents most often implicated are herpes simplex virus and human papillomavirus. These viruses appear to serve as cofactors in the inducement of various genital cancers, working together or with environmental agents such as diethylstilbestrol and host-related genetic abnormalities. The prognosis of vaginal cancer depends on the stage of the disease, with an overall 5-year survival rate of 80% to 90% for early stages.

Adenocarcinoma↗