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| REVIEW ARTICLE |
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| Year : 2022 | Volume
: 8
| Issue : 2 | Page : 82-85 |
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Cohabitation of tuberculosis and human papillomavirus-positive infections in the development of cervical cancer
Aayush Raj1, Harshath Parves1, Ashish Kumar1, B Prabasheela1, Sivanesan Dhandayuthapani2
1 Department of Pharmaceutical Engineering, Aarupadai Veedu Institute of Technology, Paiyanoor, Tamil Nadu, India
2 Central Research Facility, Santosh Deemed to be University, Ghaziabad, Uttar Pradesh, India
| Date of Submission | 24-Nov-2022 |
| Date of Acceptance | 25-Nov-2022 |
| Date of Web Publication | 11-Jan-2023 |
Correspondence Address:
B Prabasheela
Department of Pharmaceutical Engineering, Aarupadai Veedu Institute of Technology, Paiyanoor, Kancheepuram, Tamil Nadu
India
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/sujhs.sujhs_40_22
Tuberculosis (TB) has been implicated in the pathogenesis of malignancies and may interfere with their diagnosis. TB and cancer frequently coexist and the relative immunosuppression caused by cancer or its treatment may lead to the reactivation of latent TB infections, leading to increased morbidity and mortality. Human papillomavirus (HPV) infection causes cervical cancer, particularly HPV 16 and 18 strains account for 75% of these cases. Although it is difficult to determine the exact chronology of events using data from reported diagnoses of infections, it is possible to draw preliminary conclusions regarding the relationship between co-infections and HPV infection, HPV persistence, and the development of CIN3+. This review highlights the underappreciated overlap of the cohabitation of TB and HPV + ve infection in the cause of cervical cancer.
Keywords: Cervical cancer, Human papillomavirus +ve, mycobacterium, tuberculosis
How to cite this article:
Raj A, Parves H, Kumar A, Prabasheela B, Dhandayuthapani S. Cohabitation of tuberculosis and human papillomavirus-positive infections in the development of cervical cancer. Santosh Univ J Health Sci 2022;8:82-5 |
How to cite this URL:
Raj A, Parves H, Kumar A, Prabasheela B, Dhandayuthapani S. Cohabitation of tuberculosis and human papillomavirus-positive infections in the development of cervical cancer. Santosh Univ J Health Sci [serial online] 2022 [cited 2023 May 30];8:82-5. Available from: http://www.sujhs.org/text.asp?2022/8/2/82/367575 |
| Introduction | |  |
Association between malignancies and tuberculosis (TB) has been well-established for years ago.[1] TB has been implicated in the pathogenesis of malignancies and may interfere with their diagnosis. TB and cancer frequently coexist, and the relative immunosuppression caused by cancer or its treatment may lead to the reactivation of latent TB infections, leading to increased morbidity and mortality.[1] However, data on the association between cervical cancer and TB are scarce.[2] Importantly, the impact of these pandemics related to human papillomavirus (HPV) and TB is more severe in countries with more challenging health-care systems where TB and other viral infections such as HIV and HPV are less controlled and patients may have more advanced disease states compared with the developed world. TB has been implicated in the pathogenesis of malignancies and may interfere with their diagnosis. TB and cancer frequently coexist and the relative immunosuppression caused by cancer or its treatment may lead to the reactivation of latent TB infections, leading to increased morbidity and mortality.[1] However, data on the association between cervical cancer and TB are scarce.[2] Therefore, recognizing the devastating impact of the colliding HPV and TB pandemics in resource-limited settings and addressing the need for treatment is very much important.
| Tuberculosis | | |
Mycobacterium tuberculosis (MTB) caused TB remains a global dominant cause of mortality and morbidity, although treatment and preventive measures are available.[3] Globally, TB is one of the dominant causes of mortality from a single infectious disease agent, responsible for roughly 40% of deaths.[4] Worldwide, approximately, 10 million new cases of TB and about 1.57 million TB-induced deaths were reported in 2017, with incidence and mortality highest in South-Eastern Asia and Africa.[4] Estimates have equally shown that about one-fourth of the world's population is infected with latent TB and is at risk of progression to active TB.[5]
Cervical cancer
The fourth most frequently occurring cancer among women worldwide is reported as “cervical cancer:[6] One-fourth of the global burden of cervical cancer is reported to occurring in India[7] that accounts for 17% of cancer deaths among women during their reproductive age group compared to the other developed countries.[6] An earlier study by Kaarthigeyan et al. in the year 2012 reported that HPV infection causes cervical cancer, particularly HPV 16 and 18 strains account for 75% of these cases.[8]
Epidemiology
Evidences have proven that 80% of global cancer cases are attributed to oncogenic HPV.[9] A recent study by[10] revealed that prior TB infection is mostly common among patients with cases of cervical cancer,[11] also reported that TB infection is associated with high vulnerability to oncogenic HPV infection. According to,[8] oncogenic HPV and TB always coexist, and the immune suppression caused by cancer (which is a consequence of oncogenic HPV) can result in latent TB reactivation hence, leading to high mortality.[10] In addition, persistent gynecologic TB infection, resulting in chronic inflammation, could be a high-risk factor in the progression of oncogenic HPV infection to cervical cancer.[10] An association between malignancies and TB was previously established.[1] TB has been implicated in the pathogenesis of malignancies and may interfere with their diagnosis. TB and cancer frequently coexist and the relative immunosuppression caused by cancer or its treatment may lead to the reactivation of latent TB infections, leading to increased morbidity and mortality.[1] However, data on the association between cervical cancer and TB are scarce.[2]
Etiology
Having multiple sexual partners, early age of sexual intercourse, tobacco consumption, prolonged use of oral contraceptive pills, increased parity, and early age of giving birth are considered to be the most important risk factors for acquiring HPV infection.[12] Most of genital HPV infections are asymptomatic but previous research evidence shows that nearly all cervical cancer cases are caused by high-risk HPV types.[13]
| Coexistence of Human Papillomavirus Infection and Tuberculosis and Cervical Cancer | | |
Both diseases, HPV infection and TB, have a major impact on modern human health. Recently, HPV infection is reported to be one of the most common infectious diseases of the reproductive tract.[14] In addition, TB is accountable for approximately 1.57 million deaths and 10 million new infections annually worldwide.[4] Moreover, HPV and TB have accompanied mankind for a long time. MTB, the pathogen that triggers TB in most cases, has been detected in 9,000–11,000-year-old human bodies.[15],[16] Furthermore, MTB was found in ancient skeletal and mummified material,[17],[18],[19] and was first detected through a polymerase chain reaction in archaeological bone material remains of the 14th–16th century. Evidence of HPV type 18 was found in mummified tissue dating back to the 16th century.[20] However, no data or very few studies are available on the detection of HPV or MTB so far.
HPV infections are important events in the development of cervical cancer and are the focus of recent HPV vaccine development.[21] While a persistent HPV infection is widely acknowledged as a necessary precursor to cervical cancer, there is no general consensus regarding the duration of infection necessary to classify an infection as persistent or transient.[22] Persistent infection is generally classified as a woman who tests positive for HPV on two or more occasions, the interval between them ranging between 2 months and 7 or more years.[22] The rate of determined oncogenic HPV infection in SPOCCS II was estimated by assessment of oncogenic HPV infection at two-time points within a 10-month period. Given this relatively short interval, it is possible that a fraction of women classified with persistent infections may instead have transient HPV infections.
In addition, because the HC II assay does not distinguish sub-types of HPV, the women who tested positive for oncogenic HPV at both the initial and follow-up clinical screening could have been infected with either the same or different oncogenic subtypes of HPV and therefore may be transiently infected. The initial prevalence rate of HPV infection reflects either incident or preexisting infection.[23],[24] The persistence rate of oncogenic HPV infection in SPOCCS II was 15.2% and was comparable to the rate found in another study over a 7-year period.[24] The rate of persistence in this study may have been underestimated because the initial HPV diagnosis was based on the self-test, and the second HPV diagnosis was based on the direct test, with the sensitivity of the former test lower than that of the latter test.[25]
Factors influencing the odds of persistent HPV positivity included sexual behaviors, hygienic practices, and a history of infections including TB [Table 1]. Being postmenopausal rather than premenopausal was another risk factor for HPV persistence and perhaps a surrogate for age, which has been directly associated with persistent HPV infection in earlier reports.[24],[26] Although it is difficult to determine the exact chronology of events using data from reported diagnoses of infections, it is possible to draw preliminary conclusions regarding the relationship between co-infections and HPV infection, HPV persistence, and the development of CIN3+.
Host mechanisms for defense against TB and HPV both involve cell-mediated immunity. Infection with HPV and the tubercle bacilli results in chronic immune activation, followed by sustained production of inflammatory cytokines and prostaglandins,[27],[28],[29] and subsequent suppression of cell-mediated immune responses, and promotion of angiogenesis.
Chronic inflammation associated with HPV infection, TB, and other diseases may increase the production of reactive oxygen species and other potential damaging metabolites that aid carcinogenesis.[27],[28] Nutritional status may also play a role in the immunological defense against HPV infection. Many populations in Asia suffer from marginal to deficient serum levels of Vitamin A, Vitamin C, and selenium, which fluctuate with the seasonal availability of dietary-rich sources of these micronutrients.[30],[31],[32] The variation in season-specific serum levels of nutritional status has been associated with an increased risk of respiratory infections, including TB[33],[34] in children and an increased risk of lung cancer in Chinese tin miners.[35],[36] Recent evidence from SPOCCS II implicates a role for the season in HPV infection.[37] Individuals with chronic infections may have depleted nutritional stores that may increase the risk of progression from HPV infection to persistence and invasive cancer.[27],[29]
Screening with pap test or visual inspection with acetic acid or effective HPV-DNA detection procedures can be employed to easily detect the precursors of cervical cancer at an early stage and treat them efficiently. Distinct from the cancers occurring in various sites of the body cervical cancer and its precursor lesions could be detected early and is curable in the early stages of the disease. Screening women for cervical cancer is crucial as most of them do not often experience symptoms until the disease has advanced.[13]
| Conclusion | | |
The prevention and control of cervical cancer depend on awareness about the disease, screening procedures, and preventive measures.[12] Despite cancer is being included under the noncommunicable diseases control program by the Ministry of Health and Family Welfare, Government of India, there is still a need for the implementation of organized or high opportunistic screening approaches for cervical cancer in India for those patients who are reported positive for either TB and HPV + ve.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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[Table 1]
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