Detection of human papillomavirus (HPV) in genital warts and carcinomas by DNA in situ hybridization in Chinese patients

A series of 51 genital biopsies from normal epithelium, condylomata acuminata, leucoplakia and squamous cell carcinoma from Chinese male and female patients were analysed for the presence of human papillomavirus (HPV) types 6, 11, 16 and 18 by DNA in situ hybridization. All of the nine genital condyloma acuminata were positive for HPV DNA, in which HPV 6 was found in six cases, HPV 11 in two cases and HPV 18 in one case. Twelve out of the 21 cases (57.1% of the total) of cervical squamous cell carcinoma were shown to contain HPV DNA; HPV 16 was found in nine cases, HPV 18 in two cases and HPV 16/18 in one case. Present results support the earlier concept that HPV 6/11 are closely associated with benign genital lesions, and HPV 16/18 are mostly confined to higher grade of intra-epithelial neoplasias and carcinoma.     

Second primary malignancies in patients with non-melanoma skin cancer: Results from a cancer registry–based study in Emilia Romagna,north-east Italy

Backgroundprevious research on the risk of subsequent, primary non-cutaneous malignancies among patients with non-melanoma skin cancers (NMSCs) led to conflicting results. We aimed to investigate a possible link between NMSC and second primary malignancies by using the population-based data available in cancer registries.Methodsthis observational study retrospectively assessed the risk of occurrence of both synchronous and methachronous second primary tumours in a cohort of cancer patients whose first diagnosis was NMSC. The cohort came from the network of general cancer registries of the Emilia-Romagna Region, northeast Italy, in the period between 1978 and 2012, and was compared with the general population living in the same area. Two main indexes were used: i) Standardized Incidence Ratio (SIR), calculated as the ratio between the observed and the expected number of second cancers and ii) Excess Absolute Risk (EAR), expressing the absolute excess or deficit of second cancer incidence.Resultsin the period analysed (1978–2012, 72,503,157 person/years, PYs), 89,912 primary NMSC were found in 76,414 patients. Among them, 14,195 developed a second primary cancer in the subsequent 501,763 follow-up PYs. NMSC patients showed an overall SIR of 1.22 (CI 95% 1.20-1,24) and an EAR of 5.11 cases/1000 PYs (CI 95% 4.48–5.74).Conclusionsthe study results showed that NMSC patients had an increase in relative risk and, at least for some tumours, in absolute risk of developing a second cancer when compared with the general population. Genetic, environmental and personal risk factors may influence this finding.     

Human papillomaviruses and DNA ploidy in anal condylomata acuminata

Previous studies have emphasized the usefulness of DNA ploidy measurement and Human Papillomavirus (HPV) detection as prognostic markers in low grade cervical lesions. We addressed the eventual relationship between HPV type, DNA profile, and p53 tumor suppressor protein expression in anal condylomata acuminata to eventually determine parameters which may be considered as predictive risk factors for the development of cancer. DNA ploidy was assessed by image cytometry after Feulgen staining of contiguous serial sections of 45 anal condylomata acuminata without atypia containing HPV detected by in situ hybridization and Polymerase Chain Reaction (PCR). p53 expression was detected by immunohistochemistry. DNA aneuploidy was found in 53.3% of these lesions, 48.9% containing non oncogenic HPV types 6 and/or 11 and 4.4% harbouring HPV types 11 and 18. The DNA diploid lesions were all associated with non oncogenic HPV types 6 and/or 11 and one case also contained HPV type 33. There was no significant correlation between the detection of DNA aneuploidy and the presence of immuno-detected p53. DNA aneuploidy was not related to the presence of oncogenic HPV in anal condylomata acuminata. The DNA aneuploid profile frequently observed, especially in lesions associated with non oncogenic HPV types, is not yet well explained and cannot be considered as a prognostic factor. In contrast, a more intensive clinical follow-up should be proposed in patients with oncogenic HPV associated to DNA aneuploidy.     

人乳头瘤病毒感染与肿瘤的相关性研究进展

人乳头瘤病毒(Human papillomavirus,HPVs)是一种嗜人体皮肤和黏膜的DNA病毒,约80%有性行为的女性可能感染HPV。宫颈癌是最常见的恶性肿瘤之一,是女性肿瘤中仅次于乳腺癌的第二个常见的恶性肿瘤,高危型HPV感染是其主要致病因素,则宫颈癌是目前唯一病因明确的妇科恶性肿瘤。HPV感染亦与其他恶性肿瘤的发生、发展密切相关,可引起除宫颈癌外的其他泌尿生殖道肿瘤,以及消化道系统、呼吸道系统、眼科、皮肤等其他系统或器官肿瘤。对HPV感染所致肿瘤的相关研究进展进行了综述,为肿瘤病因和发生机理的研究提供了新的思路。     

Biology of human papillomavirus (HPV) infections and their role in squamous cell carcinogenesis

Current data implicating the role of human papillomavirus (HPV) infections in squamous cell carcinogenesis may be summarised as follows: animal models have shown that PVs can induce malignant transformation; HPV involvement in both benign and malignant human squamous cell tumours has been demonstrated by morphological, immunohistochemical and DNA hybridisation techniques; HPV infections in the genital tract are venereally transmitted and are associated with the same risk factors as cervical carcinoma; the natural history of cervical HPV lesions is similar to that of CIN, namely, they have the potential to develop into carcinoma in situ; malignant transformation of PV-induced lesions seems to depend on virus type and the physical state of its DNA, e.g., whether or not it is integrated in the host cell DNA; malignant transformation most probably requires synergistic actions between the PVs and chemical or physical carcinogens, or other infectious agents; genetic disposition (at least in animals) significantly contributes to malignant transformation; immunological defence mechanisms of the host are probably capable of modifying the course of PV infections (efficacy in man remains to be elucidated). Many details of the molecular mechanisms, however, still remain to be clarified. Although BPV1 is capable of transforming fibroblasts, the way that papillomaviruses transform epithelial cells is unclear. Which gene is capable of inducing the limited cell proliferation in benign lesions? No model systems exist to provide the answer nor to elucidate the progression to malignant cells and then to invasive cancer. Improved tissue culture systems for in vitro differentiation of keratinocytes should help in elucidating the biology of papillomaviruses and their interaction with cell division and differentiation.     

Long term risk of invasive cancer after treatment for cervical intraepithelial neoplasia grade 3: population based cohort study

Objective To study the long term risk of invasive cancer of the cervix or vagina after treatment for cervical intraepithelial neoplasia grade 3.Design Prospective cohort study.Setting Swedish cancer registry.Participants All women in Sweden with severe dysplasia or cervical carcinoma in situ (equivalent to cervical intraepithelial neoplasia grade 3) treated during 1958-2002 (n=132 493) contributing 2 315 724 woman years.Main outcome measures Standardised incidence ratios with risk of cancer in the Swedish general female population as reference, and relative risks in multivariable log-linear regression model, with internal references.Results Women with previous cervical intraepithelial neoplasia grade 3 had an increased risk of invasive cervical cancer compared with the general female population (standardised incidence ratio 2.34, 95% confidence interval 2.18 to 2.50). The increased risk showed a decreasing trend with time since diagnosis for women treated later than 1970 but the risk was still increased after 25 years. An effect of age was found, with an accentuated increase in risk for women aged more than 50. The excess risk for cervical cancer associated with previous cervical intraepithelial neoplasia grade 3 has steadily increased since 1958. For vaginal cancer the standardised incidence ratio was 6.82 (5.61 to 8.21) but this decreased to 2.65 after 25 years. Adjustments in the multivariable log-linear regression model did not substantially alter these results.Conclusions Women previously treated for cervical intraepithelial neoplasia grade 3 are at an increased risk of developing invasive cervical cancer and vaginal cancer. This risk has increased since the 1960s and is accentuated in women aged more than 50. The risk is still increased 25 years after treatment.     

Human Papillomavirus-Associated Subsequent Malignancies among Long-Term Survivors of Pediatric and Young Adult Cancers

Long-term survivors of pediatric and young adult (PAYA) cancers have a high incidence of subsequent neoplasms, but few risk factors other than cancer treatment have been identified. We aimed to describe the burden of human papillomavirus (HPV)-associated malignancies among survivors of PAYA cancers to assess whether HPV infections might be a reasonable area of future etiologic research on subsequent malignancies in this population. We used longitudinal data from 9 population-based registries of the Surveillance, Epidemiology, and End Results program collected between 1973 and 2010 to assemble a cohort of individuals who were diagnosed with any cancer between the ages of 0 and 29 years and survived at least 5 years post-diagnosis. We estimated sex-specific standardized incidence ratios (SIRs) with corresponding 95% confidence limits (CL) of HPV-associated subsequent malignancies (cervical, vaginal, vulvar, penile, anal, tongue, tonsillar, and oropharyngeal). Our study population comprised 64,547 long-term survivors of PAYA cancers diagnosed between 1973 and 2010. Compared with females in the general US population, female PAYA cancer survivors had a 40% relative excess of HPV-associated malignancies overall (SIR = 1.4, 95% CL: 1.2, 1.8). Compared with males in the general US population, male PAYA cancer survivors had a 150% relative excess of HPV-associated malignancies overall (SIR = 2.5, 95% CL: 1.9, 3.4). Our findings suggest an excess of HPV-associated malignancies among PAYA cancer survivors compared with the general US population. We hypothesize that a portion of subsequent malignancies among PAYA cancer survivors may be directly attributable to HPV infection. This hypothesis warrants exploration in future studies.     

Local accumulation of FOXP3+ regulatory T cells: evidence for an immune evasion mechanism in patients with large condylomata acuminata

Condylomata acuminata derived from the infection of human papillomavirus is a common sexually transmitted disease. Although T cell-mediated cellular immunity is considered as the main arm against such infection, the regulation of T cell immune responses in genital condylomata is unclear to date. In this study, we analyzed FOXP3(+) regulatory T cells in genital condylomata of patients. The results show that FOXP3(+) regulatory T cells with suppressive function accumulated in large warts. Consistently, the immunosuppressive milieu in large warts was characterized by high expression of IL-10 and TGF-beta1 and low expression of IL-2 and IFN-gamma. The responsiveness of wart-infiltrating T cells both in vitro and in vivo can be increased by depleting FOXP3(+) T cells. The accumulation of FOXP3(+) regulatory T cells in large warts can be partly ascribed to the chemotaxis of CCL17 and CCL22, derived from Langerhans cells and macrophages in wart. Although such accumulation favors the local immunosuppression, it seems not to influence the systemic immunity. In conclusion, these findings demonstrate that FOXP3(+) regulatory T cells play an important role in genital condylomata, which has multiple implications in the comprehensive treatment of condylomata acuminata.     

Identification of human papilloma viruses in male dysplastic genital lesions

The association of Human Papillomaviruses (HPV) DNA with female genital lesions has been widely documented whereas little has been reported about male genital pathologies. The aim of this work was to investigate the presence of HPV DNA and the genotype involved in male dysplastic genital lesions. All samples were analysed by polymerase chain reaction (PCR) to amplify HPV E1 and L1 genes. The PCR products were subjected to restriction fragment length polymorphism (RFLP) to determine the HPV genotype. We analysed 209 male genital biopsies from different lesions: mostly from acuminate condylomata and from Buschke-Lowenstein tumours, Bowen papulosis, leukoplakia of the glans, scrotal lymphangioma, penile horn and penile/perianal verrucous carcinoma. Our results revealed the constant presence of viral DNA in genital condylomata, mainly associated with low risk HPV; the presence of the same genotypes was also detected in some of the examined rare pathologies.     

Appendicitis as an Early Manifestation of Subsequent Malignancy: An Asian Population Study

Background & Aims

Cancer risk after appendectomy in patients with appendicitis remains unclear. This study examined the role of appendicitis as an early manifestation harbingering the distant malignancy.

Methods

From the insurance claims data of Taiwan, we identified a cohort of 130,374 patients newly received appendectomy from 2000–2009, without cancer diagnosis. A comparison cohort of 260,746 persons without appendectomy and cancer was selected from the same database, frequency matched by age, sex, comorbidity and index year. We monitored subsequent cancers with a12-month follow-up.

Results

Over all, 1406 and 616 cancer cases were identified in the appendectomy cohort and comparisons, respectively, with all cancers incidence rate 4.64-fold higher in the appendectomy cohort (9.06 vs. 1.96 per 1000 person-months). Digestive and female genital organs harbored 80.9% of cancer cases in the appendectomy cohort. The Cox model measured site-specific hazard ratio (HR) was the highest for female genital cancers (23.3), followed by cancers of colorectum (14.7), small intestine (10.1), pancreas (7.40), lymphoma (5.89) and urinary system (4.50), all significant at 0.001 level. The HR of all cancers decreased from 13.7 within 3 months after appendectomy to 1.37 in 7–12 months after the surgery. In general, relative to the comparison cohort, younger appendectomy patients tended to have a higher HR than older patients.

Conclusions

The high incident cancers identified soon after appendectomy suggest the acute appendicitis is the early sign of distant metastatic malignancy. The risk of colorectal cancer, female genital cancer and haemopoietic malignancy deserve attention.     

Human papillomavirus infection and its role in the genesis of dysplastic and neoplastic lesions of the squamous epithelia

Extensive laboratory and epidemiological evidence demonstrate that human papillomavirus (HPV) is the major cause of squamous cervical carcinoma (SCC), its precursor lesions (cervical intraepithelial neoplasia - CIN) and several other benign and malign clinical manifestations including genital warts, condylomata acuminata, Bowenoid papulosis, vaginal, vulvar and anal intraepithelial neoplasia (VIN and AIN) and carcinoma, penile carcinoma and other squamous neoplasias of the head and neck districts. In addition, mother-to-child transmission is probably responsible for recurrent laryngeal and pulmonary papillomatosis in infants. The relevance and high level of scientific interest surrounding HPVs are related to the oncogenic potential of some viral types belonging to this family and the possibility to influence the incidence of various tumour forms likecervical carcinoma, improving the efficacy of specific screening programs or defining preventive strategies like vaccination.     

Cancer incidence in Nigeria: A report from population-based cancer registries

Introduction: Cancer has become a major source of morbidity and mortality globally. Despite the threat that cancer poses to public health in sub-Saharan Africa (SSA), few countries in this region have data on cancer incidence. In this paper, we present estimates of cancer incidence in Nigeria based on data from 2 population-based cancer registries (PBCR) that are part of the Nigerian national cancer registry program. Materials and methods: We analyzed data from 2 population based cancer registries in Nigeria, the Ibadan Population Based Cancer Registry (IBCR) and the Abuja Population Based Cancer Registry (ABCR) covering a 2 year period 2009-2010. Data are reported by registry, gender and in age groups. We present data on the age specific incidence rates of all invasive cancers and report age standardized rates of the most common cancers stratified by gender in both registries. Results: The age standardized incidence rate for all invasive cancers from the IBCR was 66.4 per 100000 men and 130.6 per 100000 women. In ABCR it was 58.3 per 100000 for men and 138.6 per 100000 for women. A total of 3393 cancer cases were reported by the IBCR. Of these cases, 34% (1155) were seen among males and 66% (2238) in females. In Abuja over the same period, 1128 invasive cancers were reported. 33.6% (389) of these cases were in males and 66.4% (768) in females. Mean age of diagnosis of all cancers in men for Ibadan and Abuja were 51.1 and 49.9 years respectively. For women, mean age of diagnosis of all cancers in Ibadan and Abuja were 49.1 and 45.4 respectively. Breast and cervical cancer were the commonest cancers among women and prostate cancer the most common among men. Breast cancer age standardized incidence rate (ASR) at the IBCR was 52.0 per 100000 in IBCR and 64.6 per 100000 in ABCR. Cervical cancer ASR at the IBCR was 36.0 per 100000 and 30.3 per 100000 at the ABCR. The observed differences in incidence rates of breast, cervical and prostate cancer between Ibadan and Abuja, were not statistically significant. Conclusion: Cancer incidence data from two population based cancer registries in Nigeria suggests substantial increase in incidence of breast cancer in recent times. This paper highlights the need for high quality regional cancer registries in Nigeria and other SSA countries.     

Trends in breast and cervical cancer in India under National Cancer Registry Programme: An Age-Period-Cohort analysis

BackgroundTrend analysis in cancer quantifies the incidence rate and explains the trend and pattern. Breast and cervical cancers are the two most common cancers among Indian women which contributed 39.4 % to the total cancer in India for the year 2020. This study aimed to report the time trends in cancer incidence of breast and cervical cancer using Age–Period–Cohort (APC) model from five Population Based Cancer Registries (PBCRs) in India for the period of 1985–2014.MethodAge-Period-Cohort model was fitted to five PBCRs of Bangalore, Chennai, Delhi, Bhopal and Barshi rural for breast and cervical cancer for 25−74 age-groups. The Estimated Annual Percent Change (EAPC) was calculated. Rate Ratio (RR) of cohort effects were estimated with a constraint of period slope to be zero (p = 0) since cohort has a stronger association with incidence than period.ResultA significant increase was noted in breast cancer in all PBCRs (EAPC, Range: Delhi, 1.2 % to Bangalore, 2.7 %) while significant decrease in cervical cancer (EAPC, Range: Bangalore -2.5 % to Chennai, -4.6 %) from all the PBCRs including Barshi rural during the period. RR estimates for breast cancer showed increasing trend whereas cervical cancer showed decreasing trend in successive birth cohorts across all five PBCRs.ConclusionIn both breast and cervical cancers, a significant age, cohort and period effect was noted in Bangalore, Chennai and Delhi. Despite period effect, the cohort effect was predominant and it may be attributed to the generational changes in risk factors among cancer breast and cervix.     

Integration of papillomavirus DNA near myc genes in genital carcinomas and its consequences for proto-oncogene expression.

DNA sequences of specific human papillomavirus (HPV) types are found integrated in the cell genome in most invasive genital carcinomas. We have determined the chromosomal localization of integrated HPV type 16 (HPV-16) or HPV-18 genomes in genital cancers by in situ hybridization experiments. In three cancers, HPV sequences were localized in chromosome band 8q24.1, in which the c-myc gene is mapped, and in one cancer HPV sequences were localized in chromosome band 2p24, which contains the N-myc gene. In three of the four cases, the proto-oncogene located near integrated viral sequences was found to be structurally altered and/or overexpressed. These data indicate that HPV genomes are preferentially integrated near myc genes in invasive genital cancers and support the hypothesis that integration plays a part in tumor progression via an activation of cellular oncogenes.     

Incidence of gynaecological cancer during the COVID-19 pandemic: A population-based study in the Netherlands

ObjectiveTo study the impact of the COVID-19 pandemic and consequent lockdown on the number of diagnoses of gynaecological malignancies in the Netherlands.MethodsWe performed a retrospective cohort study using data from the Netherlands Cancer Registry (NCR) on women of 18 years and older diagnosed with invasive endometrial, ovarian, cervical or vulvar cancer in the period 2017–2021. Analyses were stratified for age, socioeconomical status (SES) and region.ResultsThe incidence rate of gynaecological cancer was 67/100.000 (n = 4832) before (2017–2019) and 68/100.000 (n = 4833) during (2020) the COVID-19 pandemic. Comparing the number of diagnoses of the two periods for the four types of cancer separately showed no significant difference. During the first wave of COVID-19 (March-June 2020), a clear decrease in number of gynaecological cancer diagnoses was visible (20–34 %). Subsequently, large increases in number of diagnoses were visible (11–29 %). No significant differences in incidence were found between different age groups, SES and regions. In 2021 an increase of 5.9 % in number of diagnoses was seen.ConclusionIn the Netherlands, a clear drop in number of diagnoses was visible for all four types of gynaecological cancers during the first wave, with a subsequent increase in number of diagnoses in the second part of 2020 and in 2021. No differences between SES groups were found. This illustrates good organisation of and access to health care in the Netherlands.     

Human papilloma virus associated with genital infection

Genital human papillomavirus (HPV) infections are among the most common sexually transmitted diseases. HPV is associated with a spectrum of diseases ranging from benign vulgar verrucae and condylomata accuminata to malignant cancers of the cervix, vulva, anus and penis. Genital HPV is in most cases transmitted sexually, but non-sexual routes of transmission, such as perinatal and autoinoculation, are possible. Men can be a reservoir of the virus that lives in latent or subclinical form on genital mucosa. Such an asymptomatic infection may be an oncogenic factor in the development of cervical cancer Colposcopic examination of the genitalia after the application of 3-5% acetic acid is a reliable method for the identification of subclinical HPV infection. Successful therapy of anogenital warts is characterized by their complete clearance, as well as by the lack of recurrence. Current treatments do not reliably eradicate HPV infections. The diagnosis and therapy of HPV infection in men is potentially beneficial because the eradication of penile HPV infection may decrease the reservoir of the virus.     

Human papillomavirus DNA detection in Papanicolaou-stained cervical smears with a nonradioactive, in situ hybridization assay.

Archived Papanicolaou-stained cervical smears from women with different cervical pathologies were processed for human papillomavirus (HPV) DNA detection and typing with an in situ hybridization (ISH) assay that employed commercial biotinylated HPV DNA probes. Two HPV DNA probes were utilized: one included HPV genotypes 6/11 and the other, 16/18. The method yielded positive results for HPV DNA 6/11 in 5 cases with condylomata acuminata (100%) and in 2 of 47 with flat warty lesions (4.2%), whereas HPV DNA 16/18 was detected in 29/47 of the latter group (61.7%). In cases with cervical intraepithelial III or invasive squamous cell carcinoma the yield was lower: positive results for HPV DNA 16/18 were obtained in only one of the five cases with one or the other cervical pathology (20%). An analysis of the results showed that the sensitivity of the assay correlated with evidence in the Papanicolaou specimens of pathognomonic cell injury from HPV infection. In the presence of such cytologic features, HPV DNA typing was possible in 37/52 cases (65.4%). In view of the modest difficulty and relatively quick execution of the nonradioactive ISH assay, the authors believe that Papanicolaou cervical smears with cytologic changes of HPV infection could be processed by this method in order to acquire information on the HPV type or types involved in the cervical infection.     

Cancer risk in childhood-onset systemic lupus

Introduction

The aim of this study was to assess cancer incidence in childhood-onset systemic lupus erythematosus (SLE).

Methods

We ascertained cancers within SLE registries at 10 pediatric centers. Subjects were linked to cancer registries for the observational interval, spanning 1974 to 2009. The ratio of observed to expected cancers represents the standardized incidence ratio (SIR) or relative cancer risk in childhood-onset SLE, versus the general population.

Results

There were 1020 patients aged <18 at cohort entry. Most (82%) were female and Caucasian; mean age at cohort entry was 12.6 years (standard deviation (SD) = 3.6). Subjects were observed for a total of 7,986 (average 7.8) patient-years. Within this interval, only three invasive cancers were expected. However, 14 invasive cancers occurred with an SIR of 4.7, 95% confidence interval (CI) 2.6 to 7.8. Three hematologic cancers were found (two non-Hodgkin’s lymphoma, one leukemia), for an SIR of 5.2 (95% CI 1.1 to 15.2). The SIRs stratified by age group and sex, were similar across these strata. There was a trend for highest cancer occurrence 10 to 19 years after SLE diagnosis.

Conclusions

These results suggest an increased cancer risk in pediatric onset SLE versus the general population. In absolute terms, this represents relatively few events. Of note, risk may be highest only after patients have transferred to adult care.     

The interaction of high and low-risk human papillomavirus genotypes increases the risk of developing genital warts: A population-based cohort study

Cervical cancer is among the most common type of cancers in women and is associated with human papillomavirus (HPV) infection. Genital warts are also reported to be linked with HPV infection types 11 and 6. In turn, clinical characteristics and morphological features of warts may be useful in the prediction of prognosis and in making treatment decisions. Thus, we have investigated the association of high and low-risk HPVs genotype with genital wart risk, as well as pathological and cytological information in cases recruited from a population-based cohort study of 1380 patients. Patients infected with HPV genotype 6 or 11 had an increased risk of having warts, with OR of 2.34 (95% CI: 0.955-5.737, P = 0.06). Also, this association was enhanced in the presence of high plus low-risk HPV for having genital wart (OR: 2.814; 95%: 1.208-6.55, P = 0.017) and cases having high-risk HPV (OR: 2.329; 95% CI: 1.029-5.269, P = 0.042). Moreover, we observed patients with genital warts having CIN2/3, indicating the importance of informing the physician to the patient to prevent more severe lesions. Our data demonstrated that patients with both low/high-risk HPV types had an increased risk of developing genital warts and persistent infection with HPV was a necessary precursor for the increase in cervical lesions.     

Immune response in cervical dysplasia induced by human papillomavirus: the influence of human immunodeficiency virus-1 co-infection -- review

Human immunodeficiency virus (HIV-1) has become an important risk factor for human papillomavirus (HPV) infection and the development of HPV associated lesions in the female genital tract. HIV-1 may also increase the oncogenicity of high risk HPV types and the activation of low risk types. The Center for Disease Control and Prevention declared invasive cervical cancer an acquired immunodeficiency virus (AIDS) defining illness in HIV positive women. Furthermore, cervical cancer happens to be the second most common female cancer worldwide. The host's local immune response plays a critical factor in controlling these conditions, as well as in changes in the number of professional antigen-presenting cells, cytokine, and MHC molecules expression. Also, the production of cytokines may determine which arm of the immune response will be stimulated and may influence the magnitude of immune protection. Although there are many studies describing the inflammatory response in HPV infection, few data are available to demonstrate the influence of the HIV infection and several questions regarding the cervical immune response are still unknown. In this review we present a brief account of the current understanding of HIV/HPV co-infection, emphasizing cervical immune response.