Catching viral breast cancer

Abstract

We have considered viruses and their contribution to breast cancer. Mouse mammary tumour virus The prevalence of mouse mammary tumour virus (MMTV) is 15-fold higher in human breast cancer than in normal and benign human breast tissue controls. Saliva is the most plausible means of transmission. MMTV has been identified in dogs, cats, monkeys, mice and rats. The causal mechanisms include insertional oncogenesis and mutations in the protective enzyme ABOBEC3B. Human papilloma virus The prevalence of high risk human papilloma viruses (HPV) is frequently six fold higher in breast cancer than in normal and benign breast tissue controls. Women who develop HPV associated cervical cancer are at higher than normal risk of developing HPV associated breast cancer. Koilocytes have been identified in breast cancers which is an indication of HPV oncogenicity. The causal mechanisms of HPVs in breast cancer appear to differ from cervical cancer. Sexual activity is the most common form of HPV transmission. HPVs are probably transmitted from the cervix to the breast by circulating extra cellular vesicles. Epstein Barr virus The prevalence of Epstein Barr virus (EBV) is five fold higher in breast cancer than in normal and benign breast tissue controls. EBV is mostly transmitted from person to person via saliva. EBV infection predisposes breast epithelial cells to malignant transformation through activation of HER2/HER3 signalling cascades. EBV EBNA genes contribute to tumour growth and metastasis and have the ability to affect the mesenchymal transition of cells. Bovine leukemia virus Bovine leukemia virus (BLV) infects beef and dairy cattle and leads to various cancers. The prevalence of BLV is double in human breast cancers compared to controls. Breast cancer is more prevalent in red meat eating and cow’s milk consuming populations. BLV may be transmitted to humans from cattle by the consumption of red meat and cow’s milk. Conclusion The evidence that MMTV, high risk HPVs and EBVs have causal roles in human breast cancer is compelling. The evidence with respect to BLV is more limited but it is likely to also have a causal role in human breast cancer.

Chromosome breaks in breast cancers occur near herpes tumor virus sequences and explain why the cancer comes back

“…One risk factor is Epstein-Barr virus /Human herpesvirus 4 (EBV/HHV4), which exists as a latent infection in almost all humans (>90%). Although most people control EBV infection (Fina et al, 2001; Lawson and Glenn, 2021), EBV increases breast cancer risk by 4.75 to 6.29-fold according to meta-analyses of 16 or 10 studies, respectively. An analysis of 24 case-control studies showed EBV is significantly more prevalent in breast cancer tissues than in normal and benign controls (Lawson and Glenn, 2021).…”

“…Although most people control EBV infection (Fina et al, 2001; Lawson and Glenn, 2021), EBV increases breast cancer risk by 4.75 to 6.29-fold according to meta-analyses of 16 or 10 studies, respectively. An analysis of 24 case-control studies showed EBV is significantly more prevalent in breast cancer tissues than in normal and benign controls (Lawson and Glenn, 2021). Infection occurs early, with 50% of children age 6-8 already seropositive, and seropositivity increases to 89% at age 18-19 (Balfour et al, 2013).…”

“…For example, Epstein-Barr virus /Human herpesvirus 4 (EBV/HHV4) exists as a latent infection in almost all humans (>90%). Most people control EBV infection (Fina et al 2001;Lawson and Glenn 2021), Life-long infections of EBV in most people obscures potential associations with breast cancer in a few people, but some associations are undeniable. EBV increases breast cancer risk by 4.75 to 6.29-fold according to meta-analyses of 16 or 10 studies, respectively.…”

“…Breast cancer cells from biopsies of sporadic and hereditary breast cancers express latent EBV infection gene products (Ayee et al . 2020; Lawson and Glenn, 2021), even after excluding the possibility that the virus comes from lymphocytes (Lorenzetti et al . 2010).…”

“…In breast epithelial cell models, EBV infection facilitates malignant transformation and tumor formation (Hu et al, 2016). Breast cancer cells from biopsies of sporadic and hereditary breast cancers express latent EBV infection gene products (Ayee et al 2020;Lawson and Glenn, 2021), even after excluding the possibility that the virus comes from lymphocytes (Lorenzetti et al 2010). In addition, EBV activation from its latent state causes massive changes in host chromatin methylation and structure (Buschle et al 2021;Kim et al 2020;Tang et al 2012).…”