Can Lyme disease and chronic infections cause cancer?

Several studies have demonstrated a negative correlation between acute infections and the emergence of cancer; however, increasing evidence reveals that persistent infections may have a considerable effect on the development of cancer.

Modifications to the body's regular defense systems or degradation of host immunity caused by changed immunological function, genetic polymorphisms, aging, and malnutrition are examples of factors that can increase susceptibility to infections.

Studies have shown that common acute infections in adults are linked to decreased risks for melanoma, glioma, meningioma, and other cancers, and exposure to febrile infectious disorders in children is associated with a reduced risk for ovarian cancer, melanoma, and many other cancers.

Tumor formation has been linked to chronic inflammation, which is associated with a number of infectious illnesses. The mitogen-activated protein kinase pathway, the production of toxins that change the cell cycle and result in aberrant cell development, and the prevention of apoptosis are all mechanisms of carcinogenesis caused by infections.

Can acute chronic infections cause cancer?

Since the beginning of the 20^th century, there has been much discussion about the complex relationship between cancer and infectious diseases. The cause of 2.2 million newly diagnosed cases of cancer in 2012 was carcinogenic infections. Helicobacter pylori (HP) (770,000 cases), human papillomavirus (HPV) (640,000), hepatitis B virus (HBV) (420,000), hepatitis C virus (HCV) (170,000), and Epstein-Barr virus (EBV) (120,000) have been identified as the most significant infectious agents involved in the development and progression of cancer.

A wide variety of host immunological responses can be modulated by infectious pathogens and related biochemical species, which in turn may affect the initiation and progression of tumors. The mechanisms that influence carcinogenesis and are associated with infection-mediated immunity are still not fully known.

Acute and chronic infections may have various effects on the development of cancer; epidemiological research has indicated that acute infections inhibit cancer development, whereas chronic infections may promote it. Rapid onset and brief duration are the hallmarks of acute infections, which are typically accompanied by fever, the release of cytokines and other inflammatory mediators, and the production of liver acute-phase proteins.

Chronic infections may occasionally result from a weak or ineffective immune response. Alterations to normal defense systems or host immunity impairment, aberrant immunological function, genetic polymorphisms, aging, and malnutrition are among the factors that enhance susceptibility to infections. The biological traits of viruses, bacteria, and parasites, such as pathogenicity, virulence, invasiveness, infectious load, toxinogenesis, contagiousness, tenacity, and vitality, may also affect whether infections occur.

People with a higher socioeconomic level (SES) are more likely to get certain tumors, such as melanoma, colorectal, breast, kidney, testicular, and prostate cancers, and those with a lower SES are more likely to develop lung, liver, cervical, and stomach cancers. In low SES groups, there is a higher frequency of chronic infections such as HPV, HP, HBV, and HCV, which have been linked to uterine cervix, stomach, and liver cancers.

There is also a higher concurrent use of tobacco and alcohol, which causes lung and liver cancers. The decline in incidence and mortality caused by infectious diseases and the rise in death rates from cancer may be inversely related. Mastrangelo et al. reported that in Italy, cases of infections were declining and those of tumors were increasing at the same time.

Reduced activation of immune defenses against altered cells during the early stages of carcinogenesis could account for this trend. There is evidence that certain viruses, including the West Nile virus, the mumps virus, the reovirus, the Newcastle disease virus, and others, may behave as oncolytic, triggering the lysis of infected cells and activating antitumor immunity. According to epidemiological research, the production of mucin 1 (MUC1), a cell surface glycoprotein, and tumor-associated antigen, which can establish immune surveillance of ovarian cancer cells, may be the preventive mechanism in preventing ovarian cancer.

According to a study by Mink et al., White females had a higher risk for ovarian cancer, which is caused by anti-MUC1 antibodies. These findings were in line with the fact that the prevalence of ovarian cancer was increasing and that of mumps parotitis infections was declining as a result of vaccination. Poliovirus infection in colon epithelial cells may offer protection from the onset of colon cancer, according to Lehrer and Rheinstein. Poliovirus cellular receptors 13 and CD155 appear to act as mediators in decreasing the mortality rate of colon cancer caused by poliovirus infection.

In this article, a summary of the research is provided on the association between chronic infections and cancer formation and progression, as well as on the use of acute infections to prevent cancer.

Some microbes can produce DNA alterations and cause chronic infections, both of which have been linked to the growth of tumors. Immunological mechanisms, such as the induction of regulatory T-cells, the production of anti-inflammatory cytokines, and the expression of immune checkpoint regulators (cytotoxic T-lymphocyte antigen 4 [CTLA-4] and programmed cell death protein-1 [PD-1]), can be linked to the development of chronic infections and cancer. T-cells that express CTLA-4 can interact with CD80 and CD86 to prevent T-cell activation, which can result in anergy. The programmed death ligands 1 and 2, which are mostly expressed on T-cells but can also be found on tumor cells and antigen-presenting cells, can interact with PD-1 to limit T-cell activity. The "initiated cells" that are gathered over the course of life may use inflammation as a promoter to accelerate the development of cancer. DNA and other biomolecules may be harmed by the biosynthesis of biochemical and metabolic intermediates during the development of tumors and inflammatory processes, which can result in the formation of malignant lesions.

Macrophages make up a significant portion of the tumor microenvironment and often support tumor survival, angiogenesis, proliferation, and dissemination. By activating certain genes involved in cell proliferation, survival, and invasion while inhibiting growth regulators such as the tumor suppressor p5328, NF-B may initiate and advance cancer in people with persistent infections.

Low-grade mucosa-associated lymphoid tissue (MALT) lymphomas, as well as lymphomas of the stomach, intestine, bladder, larynx, lung, salivary glands, spleen, and thyroid, have all been shown to regress with antibiotic therapy. The first therapeutic strategy for low-grade stomach MALT lymphoma is HP eradication therapy.

Some lymphoma forms may be linked to HP, Campylobacter jejuni, HCV, or other bacteria. After receiving antiviral medication, the remission of benign and malignant lesions caused by HPV has been documented. Anogenital warts and high-grade vulvar intraepithelial neoplasia have both been treated topically with imiquimod, an immune response modifier, or cidofovir, an inhibitor of viral replication, and the results have been positive (50%-60%).

Topical application of the antiviral medication AV2 demonstrated good outcomes in lowering the size of cervical lesions linked to HPV31 in a phase II randomized controlled trial. These results must be verified in other well-designed trials, though.

Cancer and viral infections

Viruses have the power to change the physiological processes that control growth arrest and apoptosis in the host cell. Oncogenes from biological genes involved in mitogenic signaling, cell proliferation, and programmed cell death are carried by transforming viruses.

The numerous stages of carcinogenesis may involve shared pathways among cancer-causing viruses, including HBV, HPV, and EBV, as well as the functional inactivation of p53 by virally encoded oncoproteins.

As several years may pass between the initiation of an infection and the development of cancer, host immunity may affect tumor growth. The carcinogenesis process can also be influenced by direct and indirect processes, such as potential synergies between viruses and environmental cofactors.

Seven viruses, namely, EBV, Kaposi's sarcoma-associated human herpes virus (KSHV), HPV, MCPV, HBV, HCV, and human T-cell leukemia virus type 1, have so far been identified as being linked to various types of human cancer.

Cancer and bacterial infections

Numerous factors, such as the host immune response, stimulation of cell growth, inhibition of apoptosis, and generation of bacterial toxins, may affect how bacterial infections affect carcinogenesis. Reactive oxygen and nitrogen intermediates are released during some bacterial infections that increase inflammation or hyperplasia, and these intermediates can directly result in DNA damage.

Bacterial infections may affect how carefully signal pathways in host cells are regulated, which is important for the initiation or suppression of cancer. Numerous effector chemicals produced by bacteria interact with host cells to control adhesion, alter cytoskeletal or junctional function, and activate particular eukaryotic signaling pathways.

These virulence factors can promote cancer by directly affecting cellular functions. An essential step in the growth of cancerous cells is the suppression of apoptosis, particularly when intracellular microorganisms are the cause of infections. This is typically caused by various extracellular stimuli, which are reflected by the release of tumor necrosis factor (TNF) and the serine protease granzyme B by CD8+ T-cells. High NF-B concentrations can prevent TNF-induced apoptosis.

Bacteria may help altered cells escape the destruction mechanisms by blocking apoptosis, favoring carcinogenesis. Rho family proteins can be activated by Escherichia coli cytotoxic necrotizing factor, and cyclooxygenase-2 (COX-2) can be activated by Pasteurella multocida toxin, a potent mitogen for quiescent cells and an inducer of anchorage-independent growth. COX-2 is also involved in various stages of carcinogenesis, including the suppression of apoptosis. In people with HP infection, histological changes (such as metaplasia) have been noted before the development of stomach cancer.

High salivary levels of Capnocytophaga gingivalis, Prevotella melaninogenica, and Streptococcus mitis have been found in cases of oral squamous cell carcinoma, showing diagnostic sensitivity and specificity of 80%-90%. This suggests that the presence of bacteria may be used as a diagnostic marker for cancer. The reduction of lesions following antibiotic therapy, as seen after HP eradication in patients with gastric cancer, may provide additional insight into the relationship between bacteria and cancer.

Lyme disease and the risk for leukemia

Leukemias are malignancies that affect certain immunological, bone marrow, or blood cells in the body. People can contract Lyme disease, a bacterial disease, from tick bites. Despite the stark differences between these illnesses, there may be some correlations.

Leukemias are tumors that arise from certain cells called leukocytes. Some people’s leukocytes develop and divide erratically when they have leukemia. These tumors can be categorized by medical professionals based on whether they affect lymphoid or myeloid cells. These cells belong to the leukocyte class.

Leukemia may have a wide range of genetic and environmental causes.

Small, blood-feeding arthropods known as ticks have the potential to spread the Borrelia burgdorferi bacterium. B. burgdorferi causes Lyme disease, which occurs following a tick bite, through which the bacteria can enter a person's body.

Leukemia and Lyme disease do not particularly share a direct link. However, some data suggest that Lyme disease may increase the chances of lymphoma, a different type of blood cancer, in a person. This could be a result of the body's inflammation caused by Lyme disease.

Lyme disease and lymphoma

There is some evidence that Lyme disease increases the risk for lymphomas. However, this danger is minimal, and the connection is unclear.

Different types of cancer that affect a person's lymphoid cells are known as lymphomas. These cells are a part of the immune system, and lymphomas are among the immune system's most prevalent tumors.

According to the American Cancer Society (ACS), some European people who contracted the Lyme disease-causing B. burgdorferi infection also acquired cutaneous lymphomas. However, the ACS cautions that cutaneous lymphomas are uncommon in people with Lyme disease.

Cancer as a result of Lyme disease inflammation

Scientists have proven that bacterial infections like Lyme disease may increase a person's risk of developing cancer by causing inflammation in the body. Infections and inflammation may account for up to 25% of cancer-causing factors. Although scientists are unsure of the exact mechanism at play in this process, one theory holds that inflammation damages DNA, which might result in genetic alterations that cause cancer.

Leukemia and Lyme disease occur together

Leukemia and Lyme disease can occur in a person at the same time. This person can show signs of both diseases. Leukemia and Lyme disease symptoms may overlap and be unique to each individual, so not everyone will have the same symptoms.

Common signs and symptoms of leukemia

Depending on the type of leukemia a person has, leukemia symptoms might change. Common signs and symptoms of leukemia include:

Lethargy
Fever
Chills
Easy bleeding
Easy bruising
Persistent lethargy, tiredness, and weakness
Shedding pounds without trying
Swollen lymph nodes, the liver, or the spleen
Simple bruising or bleeding
Frequent nosebleeds
Skin lesions that appear as red spots called petechiae
Excessive perspiration, especially at nighttime, is called night sweats
Muscle aches
Pain and/or tenderness in the bones

Common signs and symptoms of Lyme disease

The tick bite site develops a "bull's-eye" rash, fever, and other flu-like symptoms such as malaise, headaches, and dizziness.
Chest pain
Heart flutters
Aching or swollen joints
Enlarged lymph nodes
Neurological deficits
Brain fog

Treating leukemia and Lyme disease

The most common therapy for Lyme disease is antibiotics. For a period of 10-14 days, a doctor may advise taking antibiotics against Lyme disease.

This therapy is thought to be equally effective for people with and without leukemia, according to scientists. In patients with leukemia, it does not increase the risk for other problems.

Can Lyme disease mask leukemia, resulting in misdiagnosis?

It is unlikely that Lyme disease could conceal leukemia because the common symptoms of both illnesses differ. Some leukemia patients experience skin rashes. Under the skin, blood vessels burst, causing this to occur. When a leukemia rash appears, some people worry that Lyme disease is the cause. But the "bull's eye" rash that occasionally occurs with Lyme disease can be easily recognized. About 70%–80% of patients with Lyme disease have a rash.

It is also highly unlikely and doubtful that medical personnel would confuse Lyme disease for leukemia because the two conditions have different symptoms and operate in very different ways.

If a person has a new rash and is worried about it, they should see their doctor.

What you should talk about with your physician

A person should consult their doctor if they have any concerns about having Lyme disease. When diagnosing Lyme disease, clinicians must consider a number of variables, according to the Centers for Disease Control and Prevention. These consist of:

relevant symptoms or signs
the likelihood that a person came into contact with a tick that was carrying B. burgdorferi and the possibility of another illness with comparable symptoms
laboratory test findings

Even in the absence of a certain diagnosis, treatment for Lyme disease might begin.

Patients with leukemia and Lyme disease may also want to talk about the medical implications of having both diseases. Typically, antibiotics are used to treat Lyme disease, which is normally safe for a person with leukemia to consume.

It is important to note that Lyme disease is not contagious—it does not spread from person to person, and the bacteria can only be transmitted through tick bites.

Takeaway

Infection by bacteria, parasites, or viruses and tissue inflammation such as gastritis, hepatitis, and colitis are recognized risk factors for human cancers at various sites.

Nitric oxide (NO) and other oxygen radicals produced in infected and inflamed tissues could contribute to the process of carcinogenesis by different mechanisms, which are discussed on the basis of studies on liver fluke infection and cholangiocarcinoma development.

A similar mechanism could apply to other suspected and known cancer-causing agents, including Helicobacter pylori infection (causing stomach cancer) or Lyme disease or asbestos exposure (lung mesothelioma).

Studies on the types of tissue and DNA damage produced by NO and other reactive oxygen species are shedding new light on the molecular mechanisms by which chronic inflammatory processes may initiate or enhance carcinogenesis in humans.

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