Vol. 17 No 2 | Winter 2015
Women's Health -> Q&A
Q&a: HPV and throat cancer
Dr Min Karen Lo
Mr Julian White

This article is 9 years old and may no longer reflect current clinical practice.

For the broader O&G Magazine readership, balanced answers to those curly-yet-common questions in obstetrics and gynaecology.


‘My patient has cervical HPV and asks if she or her partner are at risk of throat cancer. What should I tell her?’

Recently, many people have become aware of information in the media suggesting that there is a link between human papillomavirus (HPV), which might be transmitted by oral sex, and oropharyngeal cancer. Little is known about the natural history of oropharyngeal HPV, but it is an area of rapidly emerging new knowledge. In common with anogenital HPV-related disease, a viral aetiology for oropharyngeal cancer raises questions for the patient, their partner and health practitioners. Common concerns are how the virus is transmitted, whether there have been sexual partners outside of the couple and how to manage an ongoing sexual relationship. It is important to emphasise that a diagnosis of HPV-related cancer does not necessarily imply multiple sexual partners or other partners outside the relationship. There is no need to alter sexual activity with a stable partner, as sharing of HPV would have occurred long before the clinical appearance of the cancer.

Does HPV cause throat cancers?

HPV is now responsible for the majority of oropharyngeal squamous cell cancers (OSCC).2,3,4 Smoking has traditionally been the most common cause of head and neck cancers. However, in the last 30 years the incidence of smoking-related head and neck cancer has declined in most countries. This has coincided with an increasing incidence of HPV as the aetiological factor in these cancers, including in New Zealand.1 In the oropharynx (tonsils and base of tongue), up to 72 per cent of OSCC cases are now attributable to HPV.2,3,4

The latency after HPV infection is typically at least ten years and can be several decades. OSCC can present with throat symptoms and an ulcerated or non-ulcerated mass visible on oral examination. However, many patients have lateral cervical lymph node metastases at the time of diagnosis and, not infrequently, a neck mass is the only clinical finding at diagnosis. Therefore, HPV-related OSCC should be considered in any patient, particularly a man, presenting with a painless lateral neck mass. The prognosis for patients with HPV-related oropharyngeal cancer is much better than for those with HPV-negative, smoking-related oropharyngeal cancers.9,10

How common is throat cancer?

Not only is the proportion of OSCC cases that are HPV-positive rising, but the incidence of OSCC is also rising. OSCC is approximately four-times more common in men than in women.1,4 In the US, the rate of OSCC in men (ten per 100 000) is now higher than the rate of cervical cancer in women (four to five per 100 000).1 In New Zealand, the rate of OSCC in men in 2012 was four per 100 000 compared to a rate of cervical cancer in women of seven per 100 000 (statistics from New Zealand cancer registry).

Why is it more common in men?

The exact reason for this gender predilection is not clear; putative reasons are a greater viral load in the female genital tract and a greater immune response in women than in men.8 The epidemiology that has been published does not differentiate between heterosexual men and men who have sex with men (MSM).

Does oral sex cause throat cancers?

Oral sex itself doesn’t cause cancer, however, oral sex is strongly associated with oral HPV infection and increased odds of OSCC. Many people have oral sex, but few develop throat cancers. Between the ages of 15–44, 80 per cent of people have had oral sex, and so far it appears only a very small percentage of the population will develop throat cancers.

What are the risk factors for OSCC?

The HPV subtypes implicated in OSCC are similar to those involved in cervical cancer. HPV 16 is implicated in up to 90 per cent of HPV cases.3,5 A strong correlation is seen between higher numbers of oral sexual partners and the development of OSCC, particularly with six or more lifetime sexual partners.6,7 Other features of sexual behaviour, which are less strongly associated include younger age at sexual debut, history of genital warts or sexually transmitted infections, rare or non-use of condoms and oral-anal sex.7

Possible other co-factors are smoking, chewing tobacco, having a weakened immune system, poor oral hygiene and conditions causing chronic irritation to the throat. Chronic irritation of the throat may be caused by chemicals irritants such as alcohol or acid reflux, and chronic bacterial tonsillitis.

Is there a test for oral HPV?

There is no routine test to diagnose oral HPV and there is no recommended screening for it. As yet, there is no guidance on what the results of oral HPV DNA test mean or how to interpret this.

What about prevention?

In contrast to cervical cancer, no clinically apparent premalignant condition exists in the vast majority of patients. Similarly, there is no reliable laboratory screening test. Therefore, there is currently no indication for population screening for HPV-related head and neck disease.11,12 This is an increasingly prevalent disease, however, and increased awareness of the disease among health professionals and the general population is to be encouraged. Limiting the number of sexual partners, delaying the onset of sexual activity and using barriers such as condoms and latex dams while performing oral sex, may be expected to minimise the risk of developing HPV-related oropharyngeal cancer.

HPV vaccination holds great promise as a mechanism for preventing the development of benign and malignant head and neck HPV-related disease. Vaccination of both boys and girls prior to the onset of sexual activity is strongly recommended.12

What is the risk to partners?

In attempting to address this, it is important to put things in context and address some of the wider issues regarding HPV. The patient who is asking this question may be anxious that she will transmit HPV to her partner. It is important to explain that:

  • More than likely, he already has been exposed to HPV. Sharing of HPV would have occurred long before the abnormal smear result or clinical appearance of a lesion.
  • It is not possible to know how long ago or from whom HPV was acquired.
  • Most sexually active people get HPV at some time in their lives, although most never know it.
  • In a long-term relationship, HPV does not imply other sexual contacts and there is no need to alter sexual practice.
  • In a new relationship, barrier protection could be considered, but one would normally encourage safe sex practices anyway in any new relationship.
  • HPV virus can develop long periods of latency and then reactivate.
  • Most individuals will become undetectable by DNA testing within one or two years.
  • Most people who acquire HPV do not develop health problems from it.
  • Partners of women with high-risk HPV (as opposed to low-risk types) can be made aware of the possibility of oropharyngeal cancer, even though the risk is low, and the possible clinical presentations.
  • The risk of a male partner for throat cancer is really independent of the fact his partner has HPV. His risk of developing OSCC depends on whether the HPV is a high-risk type (in particular HPV 16) and his own lifetime risk factors such as smoking, lifetime number of sexual and oral sex partners, oral hygiene and conditions that cause chronic irritation.

While it is helpful to normalise a diagnosis of a viral sexually transmitted infection, it is important not to unintentionally be dismissive of the potential for psychological morbidity. The way to do this is to proactively provide information and education and address key concerns.

The website provides an excellent NZ-based resource for information for both health professionals and patients, including downloadable patient information, telephone and email counselling.


  1. Chaturvedi AK, Engels EA, Pfeiffer RM, et al. Human papillomavirus and rising oropharyngeal cancer incidence in the United States. J Clin Oncol 2011;29:4294- 4301.
  2. Chaturvedi AK, Engels EA, Anderson WF, et al. Incidence trends for human papillomavirus-related and unrelated squamous cell carcinomas in the United States. J Clin Oncol 2008;26:612-9.
  3. Steinau M, Saraiya M, Goodman MT, et al. Human papillomavirus prevalence in oropharyngeal cancer before vaccine introduction, United States. Emerging Infectious Diseases 2014;20:822-8.
  4. Gillison ML, Broutian T, Pickard RK, et al. Prevalence of oral HPV infection in the United States, 2009-2010. JAMA. 2012;307:693-703.
  5. Kreimer AR, Clifford GM, Boyle P, Franceschi S. Human papillomavirus types in head and neck squamous cell carcinomas worldwide: a systematic review. Cancer Epidemiol Biomarkers Prev. 2005;14:467-75.
  6. Fakhry C, Westra WH, Li S, et al. Improved survival of patients with human papillomavirus-positive head and neck squamous cell carcinoma in a prospective clinical trial. J Natl Cancer Inst. 2008;100:261-9.
  7. Heck JE, Berthiller J, Vaccarella S, et al. Sexual behaviours and the risk of head and neck cancers: a pooled analysis in the International Head and Neck Cancer Epidemiology (INHANCE) consortium. Int J Epidemiol. 2010;39:166-81.
  8. D’Souza G, Cullen K, Bowie J, Thorpe R, Fakhry C. Differences in oral sexual behaviors by gender, age, and race explain observed differences in prevalence of oral human papillomavirus infection. PLoS One. 2014;9:e86023.
  9. Ang KK, Harris J, Wheeler R, et al. Human papillomavirus and survival of patients with oropharyngeal cancer. N Engl J Med 2010;363:24-35.
  10. Gillison M, Zhang Q, Jordan R, et al. Tobacco smoking and increased rate of death and progression for patients with p16-positive and p16-negative oropharyngeal cancer. J Clin Oncol. 2012;30:2102-2111.
  11. Kreimer AR. Prospects for prevention of HPV-driven oropharynx cancer. Oral Oncol. 2014;50:555-9.
  12. Fakhry C, D’Souza G. Discussing the diagnosis of HPV-OSCC: common questions and answers. Oral Oncol. 2013;49:863-71

One Comment

smith patterson

“HPV” includes a family of over 200 viruses. It is transmitted through direct contact. Most of us are exposed to these viruses once we become sexually active. Usually, we clear the virus through our immune system without even realizing its presence. In a minority of individuals, the virus evades our detection system and stays inside our cells for years. It may then cause warts, benign tumors or on rare occasions, cancer.


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