Oral cancer viruses

It occurs mostly in children, but can also affect adults. The association with enteroviruses primarily concerns the type A viruses, e. Coxsackie virus A16 and enterovirus, but other enteroviruses may also be involved. Herpangina is a related condition where the clinical manifestation is primarily in the oral cavity in the form of ulceration and blisters. Again, the condition is rare and restricted to children. Viral diagnostics have become more relevant in clinical dentistry.

This is partly because of an increased awareness that viruses are possible aetiological agents, and partly because the methods of viral detection have become considerably easier. The preferred methods are based on variants of real-time PCR, which not only offer a test for the viral presence, but also yield quantitative data.

The latter point is particularly relevant as several of the viruses in the oral cavity may be prevalent even in healthy mouths. A high viral load in a sample taken from affected tissues may, however, as a rule of thumb, suggest direct involvement in the underlying condition. One problem is that several viruses that are chronically present in the body can replicate in leukocytes e. As the typical clinical samples will stem from inflamed tissues, such as periodontal pockets or ulcerations, one would expect a presence of these viruses; if for no other reason due to the accumulation of leukocytes; a point that has been demonstrated at least in the case of CMV and periodontitis Again, a clinical role is suspected if the titre is particularly high, and even more so if the condition improves upon antiviral treatment.

In order to take samples for detection of viral nucleic acids, whether by PCR or other methods, it is preferable to immediately transfer the sample to a small tube containing lysis buffer. The tubes are advised to be frozen unless the samples are to be tested within a day or two, in which case they may be kept in the refrigerator. Standardisation of sampling is a challenge in connection with oral disease.

Whether the samples consist of saliva, brush scrapings from mucosa, dental plaque or subgingival plaque, both the actual amount of sample and the content, e. Theoretically, one might correlate the presence of virus with other markers in the sample, such as bacterial 16S rRNA or human genes, but that does not offer a convincing standardisation. It seems that the best option is to be careful as to adding relevance to minor amounts of virus, or small differences between samples; however, major differences such as in the antiviral treatment study 14 cannot be due to sampling variations.

A main limitation of PCR-based methods is that they only detect the viruses they are designed to detect. Several novel human viruses have appeared during the last decade, and most likely the human body is the host to a range of viruses that are yet to be described.

Moreover, the cost of the methods restricts analyses to a few viral species; thus the total spectrum of potentially relevant viruses is rarely tested. Two recent strategies compensate for this limitation: microarrays and pyrosequencing. In microarrays, probes detecting different viruses or other agents can be applied to a slide and the sample DNA or RNA hybridised onto the slide, thus offering the possible detection of all known viruses.

In pyrosequencing, the complete nucleic acids present in the sample are sequenced to look for recognisable viral sequences by searching relevant databases. Both these methods have the same, twofold limitations: one, they are less sensitive than PCR; and two, they are considerably more expensive, although the costs for pyrosequencing is becoming more cost-efficient.

Thus, these techniques are not useful for routine diagnostics, but they may be valuable when investigating a possible viral cause of unknown conditions. One such case is the common apthous ulcers, also known as canker sores. Although various viruses have been implicated by the association 28 , it seems unlikely that the true viral culprit, if any, is yet to be found.

There is no conflict of interest in the present study for any of the authors. National Center for Biotechnology Information , U. Journal List J Oral Microbiol v. J Oral Microbiol. Published online Feb Author information Article notes Copyright and License information Disclaimer.

Email: on. This article has been cited by other articles in PMC. Abstract The focus has traditionally been on bacteria and fungi when discussing microbiological aspects of oral disease. Keywords: virology, periodontitis, cancer, herpesvirus, papillomavirus, enterovirus. Clinical virology The process of evolution has shaped viruses towards the same objective as other organisms, that is, survival and procreation.

Table 1 Schematic presentation of clinical symptoms caused by viruses. Open in a separate window. The herpesvirus family Herpesviruses have a double-stranded DNA genome and are among the largest and most complex human viruses.

Table 2 Classification of human herpesviruses HHV and their associated diseases. Type Primary target cell Oral affection Other pathology 1. Herpes simplex virus-1 Mucoepithelial Herpes ulcers Genital ulcers 2.

Herpes simplex virus-2 Mucoepithelial Herpes ulcers Genital ulcers 3. Varicella Zoster virus Mucoepithelial Possible oral manifestations of chicken pox and herpes zoster Chicken pox, herpes zoster 4.

Epstein-Barr virus B-cells and epithelial cells Hairy leukoplakia, periodontitis, nasopharyngeal carcinoma Mononucleosis, lymphoma 5. Cytomegalovirus Monocytes, lymphocytes and epithelial cells Periodontitis? Mononucleosis 6. Human herpesvirus-6 T-cells and possibly others Roseola in infants 7. Human herpesvirus-7 T-cells and possibly others Roseola in infants 8. Viral—bacterial interactions Herpesviruses are well known for their capacity to manipulate the immune system.

For example, the viruses produce cytokine mimics designed to modulate the host's immune defence It should be noted that the microbial activity can also induce viral replication, as has been shown recently in the case of EBV and malaria Enteroviruses The enteroviruses belong to the family of picornaviruses. Detection of viruses in the oral cavity Viral diagnostics have become more relevant in clinical dentistry. Conflict of interest and funding There is no conflict of interest in the present study for any of the authors.

References 1. Defining the normal bacterial flora of the oral cavity. J Clin Microbiol. Slots J. Oral viral infections of adults. Periodontol J Med Virol.

Arch Virol. The role of polyomaviruses in human disease. Grinde B, Olsen I. Do cytomegalovirus or Epstein-Barr virus play a role in periodontitis? In: Gluckman TR, editor. Herpesviridae: viral structure, life cycle and infections. New York: Nova Science; In oral cancers, we are primarily concerned with HPV number 16 which is also associated with cervical, anal, and penile cancers besides those of the oropharynx.

You can have HPV without ever knowing it because the virus often produces no signs or symptoms that you will notice, and the immune response to clear it is not a process that you will be aware of. Of those approximately are HPV The vast majority of individuals will clear the virus naturally through their own immune response, and never know that they were exposed or had it.

A person can have HPV for many years, even decades, before it is detected or it develops into something serious like a cancer. In the vast majority of infected people, even with a high-risk version of HPV known to cause cancers, they will not develop cancer.

Testing positive for an HPV infection does not mean that you or your partner is having sex outside of your relationship. It is believed to have long periods of inactivity or dormancy that may even cover decades; these are periods of time that you will test negative for it.

Sexual partners who have been together for a while tend to share all types of sexual infections. Typically if one partner has a fungal infection like Candida, the other partner has it as well, even though they may appear to be asymptomatic.

The same is true of other common sexual infections like Chlamydia, a bacterial infection. HPV viral infections also are commonly shared. This means that the partner of someone who tests positive for HPV likely has HPV already, even though they may have no signs or symptoms.

Like most Americans, their immune system will customarily clear it in under 2 years. Condoms may lower your chances of contracting or passing the virus to your sexual partners if used all the time and the right way. For most of us, this occurs late in our teens and twenties when our sexual activity is the highest and the number of partners is likely the greatest.

HPV and Oral Cancer: HPV is the leading cause of oropharyngeal cancers; primarily the tonsils, tonsillar crypt, the base of the tongue the very back of the mouth and part of what in lay terms might be called a part of the throat , and a very small number of front of the mouth, oral cavity cancers.

HPV16 is the version most responsible, and affects both males and females. More males than females will develop oropharyngeal cancers.

This understanding was elucidated and the reason revealed for it in a published study by Gillison et. Through conventional genital sex, females acquire infection early in their sexual experiences, and rapidly within very few partners, seroconvert that infection into a systemic antibody that protects them through life. Males take a far greater number of sexual partners to seroconvert an infection into a systemic protective antibody.

This increased number of partners and exposure before the development of a protective antibody against the invading virus is most likely the reason that more males will later in life develop oropharyngeal cancers than females. In public messages for simplicity, OCF frequently speaks about oral cancers in general. Scientifically, this is actually anatomically divided up into the oral cavity and the oropharynx; two distinct anatomical sites though they are one continuous space.

Each anatomical site has different statistics, infections, disease etiologies which dominate that location, and outcomes from treatment are different in each location.

The fastest growing segment of the oral and oropharyngeal cancer population are otherwise healthy, non-smoking individuals in the age range. When you consider both anatomical sites, the growth is in oropharyngeal HPV positive cancers primarily. White, non-smoking males age 35 to 55 are most at risk, 4 to 1 over females. Risk Factors: Number of sexual partners- The greater your number of sexual partners, the more likely you are to contract a genital HPV infection; and when engaging in oral sex, this also holds true for oral infections.

Having sex with a partner who has had multiple sex partners also increases your risk. Oral Cancer Signs and Symptoms: This list considers both oral cancers from HPV and those from tobacco and alcohol An ulcer or sore that does not heal within weeks A red, white, or black discoloration on the soft tissues in the mouth Difficult or painful swallowing.

In oropharyngeal cancers of the tonsil, base of tongue and the oropharynx itself, it is now the dominant cause Of interest, the percentage of HPV-positive oral cancers is reported to be increasing in several countries. This increase is attributed to changing sexual practices, suggesting that HPV-associated oral cancers, like HPV-associated anal and cervical cancer, should be considered a sexually transmitted infection. It is estimated to cause more than 1 million annual deaths worldwide, with one third of these deaths caused by Hepatocellular carcinoma and the remainder by cirrhosis.

Chronic Hepatitis B infection confers a 20 times increased risk for Hepatocellular carcinoma. Hepatitis B vaccination is now included in the standard childhood vaccination series in the United States, but immigrant and older populations can have high HBV carrier rates. Intrapartum transmission is a major cause of transmission of Hepatitis B to children. Hepititis C viral infection is another a major cause of Hepatocellular carcinoma.

Whereas the carrier rate of Hepititis C in the United States was estimated at 1. Vaccines forHepititis C are in development, but for patients who have already contracted Hepititis C, a regimen involving 6 months of pegylated interferon Hepititis C virusand aggressive attempts at eradication can therefore reduce the subsequent risk for cancer in populations at risk.

EBV is the primary cause of infectious mononucleosis, a typically benign disease of adolescence and young adulthood. Nasopharyngeal cancer affects approximately 80, people each year, predominantly in less developed countries. Most of these cases are attributable to EBV infection.

Although this cancer is curable with intensive chemotherapy and radiation therapy, most of the people affected by this cancer do not have access to these treatments. The causative infectious agent for peptic ulcer disease, H pylori, is also a known cancer-causing agent. Chronic infection with this pathogen predisposes to stomach cancer and to gut mucosa-associated lymphoid tissue MALT lymphoma.

In , it was estimated that H pylori caused as many as , cases of gastric cancer per year worldwide. Because the infection first occurs in young children, H pylori seems to be an amenable target for vaccine development to prevent colonization and subsequent stomach cancer and gut-associated MALT lymphoma.

Until a vaccine becomes available, healthcare providers should screen for dyspepsia and peptic ulcer disease and offer H pylori testing to affected patients. Healthcare providers should administer drug therapy for eradication of H pylori in those who are symptomatic and H pylori-positive. Sometimes this is sufficient to cause regression of the cancer.

In other cases, the cancer continues to spread and combination chemotherapy is required. Routine maternal prenatal testing for HBV Immediate postpartum intervention to prevent maternal to child transmission Universal vaccination of children for HBV Vaccination of all adolescents who had not received HBV vaccine previously Vaccination of adults at risk for becoming infected with HBV.

The childhood immunization schedule, a 3-vaccine series administered in the first year of life, confers long-term immunity to HBV. Infants born to HBV-positive mothers must receive both vaccination and hepatitis B immune globulin within the first 12 hours of life. Because children are at increased risk for becoming chronic carriers when infected with HBV, starting the vaccine at birth and completing the series during routine well-child visits during the first year of life decreases the risk for infection from HBV-positive household contacts.

Both vaccines are equally effective at preventing HPV infection caused by the serotypes contained in the vaccines, and both will prevent development of high-grade cervical lesions caused by the corresponding serotypes. These vaccines are most effective when given to women and girls who have not been exposed to HPV. A corresponding reduction in the number of women who required invasive surgical resection of their precancerous lesions suggests that even in older, HPV-exposed women, vaccination may be helpful in reducing cervical cancer rates.

The follow-up timeframe for these vaccines is still short, so it is not clear how long the protective effect will last. Additional postapproval studies are ongoing to determine the duration of protection and to determine whether post exposure vaccination is warranted. The availability of HPV vaccines against serotypes 16 and 18 gives healthcare providers the tools to prevent HPV infection and subsequent cervical cancer.

Whereas HPV vaccines have been approved and are being administered in the United States, the uptake of the vaccines has been uneven. A backlash against HPV vaccination has occurred in some communities, as a result of a general anti-vaccine movement spurred by misinformation.