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Infections and cancer

While cancer is not infectious there are a number of infections that can increase cancer risk. It is estimated that as many as one in ten cancer cases in the UK are caused by infectious diseases1. In many cases infectious agents can be successfully eradicated, preventing the development of cancer.

This page gives an overview of infections and cancer, including hepatitis, human papillomavirus, helicobacter pylori, human T-cell lymphotrophic virus group 1, herpes virus and human immunodeficiency virus type 1. For more detailed information on these infections see the infectious agents section.

Table 8.1 shows a summary of what we know about infections and cancer.

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Hepatitis virus and cancer

Chronic infection with hepatitis B and C causes 75 to 80% of liver cancers diagnosed worldwide2. There is also an increased risk of non-Hodgkin lymphoma (NHL) among people infected with hepatitis C.

The hepatitis viruses are spread through the exchange of body fluids, hepatitis B through unprotected sex, needle sharing and from mother to baby during childbirth. Infection can take place directly from one child to another.

Hepatitis C can be spread in the same ways but it is most commonly spread by needle sharing 3,4. Infection in childhood is rare in Europe and vaccination for hepatitis B is effective and widespread. A vaccine for hepatitis C has yet to be developed, but there are several other means used to prevent the spread of the infection2.

Prevalence of hepatitis B infection in Europe is lower than 2%, but reaches 8% or higher in parts of Africa and Asia. Rates of liver cancer reflect this distribution5. Worldwide, 0.5 to 2% of the population have current or past infection with hepatitis C6.

Infection with hepatitis D only occurs in people infected with hepatitis B. Co-infection or superinfection with hepatitis D is associated with a higher rate of development of progressive liver disease and cirrhosis. However, evidence for carcinogenicity of hepatitis D infection is currently insufficient7.

The Infectious agents section has more detailed information on hepatitis viruses.

Human papilloma virus and cancer

Human papillomavirus (HPV) is linked to risk of all anogenital cancers including, cervical cancer, vaginal cancer, vulval cancer, anal cancer, penile cancer, and others.

More than 30 types of HPV virus have been identified. Studies of antibodies to HPV in people with anogenital cancer or presence of HPV DNA in tumour samples show that HPV 16 is the most commonly detected type of the virus.

HPV and Cervical cancer

HPV DNA is found in more than 99% of invasive cervical cancer samples worldwide and infection is thought to be a necessary cause of cervical cancer. 8

Studies have reported odds ratios of 17-24 for high grade cervical pre-cancer or invasive cancer in women with high-risk HPV infection of the cervix 9, 54 , and the risk for women infected with HPV 16 is higher than 100. 54

Infection with more than one type of HPV is related to a much higher risk of high-grade pre-cancerous cervical lesions than infection with one type only.12

After HPV 16, HPV 18 is the second type most closely linked to cervical cancer, and is associated most strongly with cervical adenocarcinomas. 10,11

Prevalence of cervical HPV infection in women screened in Manchester was 23% in women under the age of 25, falling to less than 4% among women aged over 40. 9

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HPV and Vaginal cancer

Squamous cell carcinomas (SCC) are the most common type of vaginal cancer, and more than half of invasive and 80% of in situ vaginal SCC contain HPV DNA. 13

Testing positive for HPV 16 antibodies is associated with four to five-fold increased risks of in situ and invasive vaginal cancer, and risk ratios are higher if there is also evidence of HPV DNA in the tumour11,13

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HPV and Vulval cancer

SCC make up 90% of vulval cancers. Detection rates of HPV DNA in invasive vulval SCC of 20–50% have been reported. 14,15

Between 70% and 90% of in situ SCC contain HPV DNA. 15,16Testing positive for HPV 16 antibodies is associated with a five-fold increased risk of in situ vulval SCC and a three-fold increased risk of invasive vulval SCC. 11

HPV and Anal cancer

More than 80% of anal cancers contain HPV DNA. 17,18Having antibodies to HPV 16 has been associated with six-fold and four-fold increased risks of anal SCC in men and women, respectively. 18

There is evidence that anal infection with several types of HPV is related to a higher risk of anal pre-cancerous lesions compared to infection with one type only. 19

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HPV and Penile cancer

Almost 90% of in situ and 70% of invasive penile tumour samples are positive for HPV DNA. 20 Men with antibodies to HPV 16 have double the risk of invasive penile cancer of men without antibodies. 20

HPV and Other cancers

There is evidence that HPV causes oropharyngeal cancer. Risk ratios for antibodies to HPV 16 vary widely, from 3.5 to 67, depending on the study and the specific HPV 16 antibodies present21-23

A different group of HPV types associated with the condition epidermodysplasia verruciformis are linked to risk of non-melanoma skin cancer. 24-28

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Co-factors with HPV infection in carcinogenesis

Factors that facilitate the progression of HPV infection in cervical cancer include cigarette smoking, higher parity, earlier age at first intercourse and immune suppression (see human immunodeficiency virus type-1) 29,30 . Smoking also appears to interact with HPV in vulval cancer. 15

Infection with certain other sexually transmitted infections may act as a co-factor with HPV infection: A recent pooled analysis of case-control studies reported an almost doubling of risk for cervical SCC among women seropositive for herpes simplex virus-2 (HSV-2) and with HPV DNA in cervical cells compared with women positive for HPV DNA only. 31

HSV-2 infection is also associated with an increased risk of anal cancer, 18 vaginal cancer, 13 in situ vulval cancer15 and penile cancer. 20

An international multicentre case-control study reported an OR of 1.7 for SCC of the cervix in HPV positive women with serum antibodies to chlamydia trachomatis. A positive trend was reported for higher antibody titres to C. trachomatis. 32

Preventing HPV infection

A single prophylactic vaccine against HPV type 16 and 18 has been shown to be 100% effective in preventing persistent HPV infection of the cervix and 93% effective in preventing cytological abnormalities. 33

Early stage trials in women with vulval intraepithelial neoplasia have been promising, with evidence of an immune response and lesion shrinkage. 34

The Infectious agents section has more detailed information on human papillomaviruses infections.

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Helicobacter Pylori infection and cancer

Helicobacter pylori (H.pylori) causes about 60% of stomach cancers in developed countries; the bacterium invades the stomach lining, causing chronic gastritis35. The RR of stomach cancer associated with seropositivity for H. pylori ranges from 2 to almost 3036,37. The fall in rates of gastric cancer worldwide has been linked to decreasing prevalence of H. pylori infection35.

H. pylori is mainly contracted in childhood, and appears to be transmitted by close contact with others. Adults with the infection are significantly more likely to have shared a room or a bed in childhood than those without infection38.

Prevalence of H. pylori infection has been shown to fall with decreasing age in the developed world, which is thought to reflect decreasing prevalence of infection in children39. There are highly effective treatments for the infection and evidence from randomised trials suggests a reduction in gastric cancer risk with H. pylori eradication40-42.

Eradication is also an effective treatment for low grade gastric mucosa-associated lymphoid tissue (MALT) lymphomas44.

The Infectious agents section has more detailed information on helicobacter pylori infections.

Human T-cell lymphotrophic virus group 1 (HTLV-I) and cancer

HTLV-I is a known cause of adult T-cell leukaemia/lymphoma (ATLL). The virus is transmitted: from mother to child, mainly via breast feeding beyond the age of six months; by needle sharing; infected blood transfusions; or sexually.

Prevalence of HTLV-I is highest in Japan, the Caribbean Basin, parts of South America, Central and West Africa. The global prevalence of infection is estimated at 15-20 million. ATLL develops in 2 to 5% of HTLV-1-infected people and incidence is almost exclusive to areas where the infection is widespread44.

The Infectious agents section has more detailed information on HTLV infections.

Herpesviruses and cancer

More than 90% of adults worldwide are infected with Epstein Barr virus (EBV), a gamma-1 herpesvirus. Infection usually occurs in childhood and can result in infectious mononucleosis (glandular fever)45.

Global variations in the incidence of nasopharyngeal cancer are the result of interactions between environmental or genetic factors and EBV infection46.

EBV infection is also essential for the development of endemic Burkitt’s lymphoma, working as a co-factor with malaria, causes lymphomas in the immunosuppressed and is estimated to be involved in the development of more than 40% of cases of Hodgkin’s disease worldwide47. It may also be significant in development of sinonasal T-cell lymphomas45. Research is ongoing into a vaccine for EBV or infectious mononucleosis48.

Infection with human herpesvirus 8 (Kaposi’s sarcoma-associated herpesvirus, KSHV) – a gamma-2 herpesvirus – is essential for development of Kaposi’s sarcoma, and is also implicated in some AIDS-related lymphomas49.

The Infectious agents section has more detailed information on herpes virus infections.

Human immunodeficiency virus type-1(HIV-1) and cancer

Infection with HIV-1 greatly increases risk of Kaposi’s sarcoma and rates of this cancer are highest in areas where prevalence of both KSHV and HIV-1 are high49. Risk increases as immunosuppression worsens: Among people with AIDS in the southeast of England, incidence of Kaposi’s sarcoma increased 1,000-fold50.

HIV-1 also increases risk of lymphomas, HPV-associated cancers, liver cancer, leukaemia and lung cancer49-51. Most of these cancers are associated with a viral cause, and it is likely that the weakened immune system of someone with AIDS allows carcinogenic viruses to proliferate more quickly, helping the growth of tumours.

However, some AIDS lymphomas carry no evidence of infection with EBV or KSHV and may occur spontaneously as a result of chronic stimulation of the immune system49. Anti-retroviral drugs are important in preventing and treating Kaposi’s sarcoma and lymphomas in AIDS patients52,53

References for infections and cancer risk

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2. UICC Handbook for Europe: Evidence based Cancer Prevention: Strategies for NGOs. 2004.
3. Engels, E.A., et al., Hepatitis C virus infection and non-Hodgkin lymphoma: results of the NCI-SEER multi-center case-control study. Int J Cancer, 2004. 111(1): p. 76-80.
4. de Sanjose, S., et al., Role of hepatitis C virus infection in malignant lymphoma in Spain. Int J Cancer, 2004. 111(1): p. 81-5.
5. International Agency for Research on Cancer, Hepatitis B Virus: Summary of data reported and evaluation of evidence. 1994.
6. International Agency for Research on Cancer, Hepatitis C Virus: Summary of data reported and evaluation of evidence. 1994.
7. International Agency for Research on Cancer, Hepatitis D Virus: Summary of data reported and evaluation. 1994.
8. Walboomers JMM, Jacobs MV, Manos MM. Human Papillomavirus is a necessary cause of invasive Cervical Cancer Worldwide. Journal of Pathology 1999(189):12-9.
9. Peto J, Gilham C, Deacon J, et al. Cervical HPV infection and neoplasia in a large population-based prospective study: the Manchester cohort. BJC 2004;91(5):942-53.
10. Bulk S, Berkhof J, Bulkmans NW, et al.Preferential risk of HPV16 for squamous cell carcinoma and of HPV18 for adenocarcinoma of the cervix compared to women with normal cytology in The Netherlands. BJC 2006;94(1):171-5.
11. Carter JJ, Madeleine MM, Shera K, et al.Human papillomavirus 16 and 18 L1 serology compared across anogenital cancer sites Cancer Res 2001;61(5):1934-40.
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14. Kagie MJ, Kenter GG, Zomerdijk-Nooijen Y, et al.Human papillomavirus infection in squamous cell carcinoma of the vulva, in various synchronous epithelial changes and in normal vulvar skin. Gynecol Oncol 1997;67(2):178-83.
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16. Junge J, Poulsen H, Horn T, Hording U, Lundvall F.Human papillomavirus (HPV) in vulvar dysplasia and carcinoma in situ. Apmis 1995;103(7-8):501-10.
17. Frisch M, Glimelius B, van den Brule AJ, et al. Sexually transmitted infection as a cause of anal cancer. NEJM 1997;337(19):1350-8.
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19. Chin-Hong PV, Vittinghoff E, Cranston RD, et al.Age-related prevalence of anal cancer precursors in homosexual men: the EXPLORE study. JNCI 2005;97(12):896-905.
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21. Herrero R, Castellsague X, Pawlita M, et al. Human papillomavirus and oral cancer: the International Agency for Research on Cancer multicenter study. JNCI 2003;95(23):1772-83.
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24. Harwood CA, Surentheran T, Sasieni P, et al. Increased risk of skin cancer associated with the presence of epidermodysplasia verruciformis human papillomavirus types in normal skin. Br J Dermatol 2004;150(5):949-57.
25. Karagas MR, Nelson HH, Sehr P, et al. Human papillomavirus infection and incidence of squamous cell and basal cell carcinomas of the skin. JNCI 2006;98(6):389-95.
26. Masini C, Fuchs PG, Gabrielli F, et al. Evidence for the association of human papillomavirus infection and cutaneous squamous cell carcinoma in immunocompetent individuals. Arch Dermatol 2003;139(7):890-4.
27. Feltkamp MC, Broer R, di Summa FM, et al. Seroreactivity to epidermodysplasia verruciformis-related human papillomavirus types is associated with nonmelanoma skin cancer. Cancer Res 2003;63(10):2695-700.
28. Struijk L, Bouwes Bavinck JN, Wanningen P, et al. Presence of human papillomavirus DNA in plucked eyebrow hairs is associated with a history of cutaneous squamous cell carcinoma. J Invest Dermatol 2003;121(6):1531-5.
29. Mandelblatt JS, Kanetsky P, Eggert L, Gold K.Is HIV infection a cofactor for cervical squamous cell neoplasia? Cancer Epidemiol Biomarkers Prev 1999;8(1):97-106.
30. Deacon J, Evans C, Yule R, et al. Sexual behaviour and smoking as determinants of cervical HPV infection and of CIN 3 among those infected. A case-control study nested within the Manchester cohort. BJC 2000;83:1565-72.
31. Smith JS, Herrero R, Bosetti C, et al.Herpes Simplex Virus-2 as a Human Papillomavirus Cofactor in the Etiology of Invasive Cervical Cancer. JNCI 2002;94(21):1604-25.
32. Smith JS, Bosetti C, Munoz N, et al. Chlamydia trachomatis and invasive cervical cancer: a pooled analysis of the IARC multicentric case-control study. IJC 2004;111(3):431-9.
33. Harper DM, Franco EL, Wheeler C, et al. Efficacy of a bivalent L1 virus-like particle vaccine in prevention of infection with human papillomavirus types 16 and 18 in young women: a randomised controlled trial. Lancet 2004;364(9447):1757-65.
34. Davidson EJ, Boswell CM, Sehr P, et al.Immunological and clinical responses in women with vulval intraepithelial neoplasia vaccinated with a vaccinia virus encoding human papillomavirus 16/18 oncoproteins. Cancer Res 2003;63(18):6032-41.
35. Forman, D., Helicobacter pylori infection: a novel risk factor in the etiology of gastric cancer. J Natl Cancer Inst, 1991. 83(23): p. 1702-3.
36. Blaser, M.J., Helicobacter pylori and gastric diseases. Bmj, 1998. 316(7143): p. 1507-10.
37. Brenner, H., et al., Is Helicobacter pylori infection a necessary condition for noncardia gastric cancer? Am J Epidemiol, 2004. 159(3): p. 252-8.
38. Webb, P.M., et al., Relation between infection with Helicobacter pylori and living conditions in childhood: evidence for person to person transmission in early life. BMJ, 1994. 308(6931): p. 750-3.
39. Goodwin, C.S., M.M. Mendall, and T.C. Northfield, Helicobacter pylori infection. Lancet, 1997. 349(9047): p. 265-9.
40. Wong, B.C., et al., Helicobacter pylori eradication to prevent gastric cancer in a high-risk region of China: a randomized controlled trial. JAMA, 2004. 291(2): p. 187-94.
41. Uemura, N., et al., Effect of Helicobacter pylori eradication on subsequent development of cancer after endoscopic resection of early gastric cancer. Cancer Epidemiol Biomarkers Prev, 1997. 6(8): p. 639-42.
42. Ley, C., et al., Helicobacter pylori eradication and gastric preneoplastic conditions: a randomized, double-blind, placebo-controlled trial. Cancer Epidemiol Biomarkers Prev, 2004. 13(1): p. 4-10.
43. Fischbach, W., et al., Long term outcome of patients with gastric marginal zone B cell lymphoma of mucosa associated lymphoid tissue (MALT) following exclusive Helicobacter pylori eradication therapy: experience from a large prospective series. Gut, 2004. 53(1): p. 34-7.
44. International Agency for Research on Cancer. Human T-cell lymphotrophic viruses, type I and II: Summary of data reported and evaluation. 1996.
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46. Spano, J.P., et al., Nasopharyngeal carcinomas: an update. Eur J Cancer, 2003. 39(15): p. 2121-35.
47. Young, L.S. and A.B. Rickinson, Epstein-Barr virus: 40 years on. Nat Rev Cancer, 2004. 4(10): p. 757-68.
48. Andersson, J., .An Overview of Epstein-Barr Virus: from Discovery to Future Directions for Treatment and Prevention. Herpes, 2000. 7(3): p. 76-82
49. Boshoff, C. and R. Weiss, AIDS-related malignancies. Nat Rev Cancer, 2002. 2(5): p. 373-82.
50. Newnham, A., et al., .The risk of cancer in HIV-infected people in southeast England: a cohort study. Br J Cancer, 2005. 92(1): p. 194-200
51. International Agency for Research on Cancer,Human Immunodeficiency Viruses: Summary of data reported and evaluation. 1996.
52. Mocroft, A., et al., The changing pattern of Kaposi sarcoma in patients with HIV, 1994-2003: the EuroSIDA Study. Cancer, 2004. 100(12): p. 2644-54.
53. Thirlwell, C., et al.,Acquired immunodeficiency syndrome-related lymphoma in the era of highly active antiretroviral therapy. Clin Lymphoma, 2003. 4(2): p. 86-92.
54. van der Graaf, Y., Molijn, A., Doorneward, H., et al Human papillomavirus and the long-term risk of cervical neoplasia. Am J Epidemiol 2002; 156 (2); 158-64

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