Healthy cervical cells as seen under a microscope. Image: National Cancer Institute

January is Cervical Health Awareness Month. The biggest threat to cervical health is human papillomavirus, or HPV, a virus that is transmitted through a wide variety of sexual activities. If you haven’t yet been sexually active, the best thing you can do to protect cervical health (whether you have a cervix or not) is to be vaccinated against HPV. If you have been sexually active, the vaccine could still be effective, assuming you haven’t already been infected with the strains of HPV against which it protects. And, if you are, or have been, sexually active and have a cervix, it is important to be screened with regular Pap tests (also called Pap smears). When caught in its precancerous stages, cervical cancer can be avoided.

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HPV may be tiny, but it packs a punch.

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There are more than 100 strains of HPV, approximately 40 of which can be sexually transmitted; of these, 18 strains are thought to cause cancer. Chronic infections by cancer-causing HPV strains, such as HPV-16 and HPV-18 (which together are responsible for 70 percent of cervical cancers), can lead to the development of abnormal cells, which might eventually become cancerous.

In the United States, HPV is the most widespread sexually transmitted disease — 6 million Americans are infected with HPV annually, although most are asymptomatic and unaware they were infected. For most people, the infection clears up within 8 to 13 months, while for others, the infection can lurk undetected. If you are unlucky enough to develop a chronic HPV infection, then you are at increased risk for certain cancers — depending on the site of the infection, HPV can cause cancers of the cervix, anus, and other genitals, as well as the throat.

Low-grade lesions of cervical cells, which can be treated before progressing to cancer. Image: National Cancer Institute

Almost all cervical cancers (99 percent) are caused by chronic HPV infection, which is a necessary, but not sufficient, condition for cancer. For a chronic HPV infection to become cancerous, a series of events must take place at the cellular level — environmental factors, such as smoking, can increase the risk for cancer, and some people have genes that make them more vulnerable to HPV infection.

Upon transmission to a host, HPV transmits its DNA into the nuclei of skin cells called basal keratinocytes. The keratinocytes replicate the viral DNA with each cell division, and eventually there are enough virus-filled cells that HPV can be easily transmitted to a sexual partner when skin cells are shed. HPV-infected keratinocytes can also remain within the host, resulting in a chronic infection. At this stage, the viral DNA is permanently integrated with that of the host, which forces the keratinocytes to manufacture viral proteins. These proteins can cause cancer by disrupting the host’s cell cycle.

HPV may be tiny, but it packs a punch. Despite only having a handful of genes, it is able to exploit some of our biological processes at the cellular level. For instance, our bodies are able to attach a “tag” to a protein to mark it for destruction. These tagged proteins, no longer needed or wanted by the body, are broken down into smaller molecules. We also all have proteins called p53, which can suppress the formation of tumors.

Cancer-causing HPV produces a protein that is shaped in such a way that it can physically interlock with both the “tags” that mark a molecule for destruction as well as the tumor-suppressing p53 proteins. When the body sees the tag, it destroys both the viral protein as well as the p53 protein that is attached to it. Our bodies are tricked into destroying our own tumor-suppressing p53 proteins, making us that much more vulnerable to developing tumors.

Just as the above proteins are able to physically fit into and around one another, components of our immune systems work based on the same principle. Our bodies’ defenses produce proteins that attach to the outer shells of viruses, which help us to attack and destroy pathogenic invaders. Our genes affect the shapes of the defensive proteins we produce; some of us might produce proteins that are more easily able to attach to invading HPVs.

Cancerous cervical cells, as seen under a microscope. Image: National Cancer Institute

You might have heard of the BRCA mutation, in which certain types of the BRCA gene can make some people more susceptible to breast cancer than others. Researchers have found genes that are similarly involved with HPV infection, such as a gene called HLA-DRB1. If you have a “bad” version of this gene, you will be more susceptible to cervical cancer than people with “good” versions of that gene. A “good” HLA-DRB1 gene codes for a protein that is able to bind to HPV’s viral antigens and present them to the immune system. If a female has a “bad” version of HLA-DRB1 and can’t make proteins that bind to HPV’s viral antigens, her immune system might be unable to stimulate a response to HPV, making her susceptible to HPV infection and ultimately cervical cancer.

This is what we mean when we say an HPV infection is a necessary, but not sufficient, condition for the development of HPV-related cancers. Some people’s immune systems might have a harder time responding to an HPV infection than others, and they will be more likely to develop HPV-related cancer over time. This is why Pap tests are such powerful tools — by catching cellular abnormalities that might eventually turn into invasive cancer, you can be easily treated. Additionally, the HPV vaccine will protect you from the two most high-risk HPV strains.

Planned Parenthood health centers, as well as other clinics and health-care providers, offer both life-saving Pap tests as well as the HPV vaccine. These simple medical interventions are two of the best things you can do to protect cervical health.