We have considered viruses and their contribution to breast cancer. 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. 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. 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 (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. 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.

中文翻译：

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发现病毒性乳腺癌

我们已经考虑了病毒及其对乳腺癌的影响。小鼠乳腺肿瘤病毒 (MMTV) 在人类乳腺癌中的患病率是正常和良性人类乳腺组织对照的 15 倍。唾液是最合理的传播方式。MMTV 已在狗、猫、猴子、小鼠和大鼠中发现。因果机制包括插入性肿瘤发生和保护酶 ABOBEC3B 的突变。乳腺癌中高危人乳头瘤病毒 (HPV) 的患病率通常比正常和良性乳腺组织对照高 6 倍。患 HPV 相关宫颈癌的女性患 HPV 相关乳腺癌的风险高于正常人。已在乳腺癌中鉴定出挖空细胞，这是 HPV 致癌性的指示。HPV 在乳腺癌中的致病机制似乎与宫颈癌不同。性活动是最常见的 HPV 传播形式。HPV 可能通过循环的细胞外囊泡从子宫颈传播到乳房。Epstein Barr 病毒 (EBV) 在乳腺癌中的流行率是正常和良性乳腺组织对照的五倍。EBV 主要通过唾液在人与人之间传播。EBV 感染通过激活 HER2/HER3 信号级联反应使乳腺上皮细胞易于发生恶性转化。EBV EBNA 基因有助于肿瘤的生长和转移，并具有影响细胞间质转化的能力。牛白血病病毒 (BLV) 感染肉牛和奶牛并导致各种癌症。与对照组相比，BLV 在人类乳腺癌中的患病率是两倍。乳腺癌在食用红肉和食用牛奶的人群中更为普遍。BLV 可能通过食用红肉和牛奶从牛传播给人类。MMTV、高风险 HPV 和 EBV 在人类乳腺癌中具有因果作用的证据令人信服。关于 BLV 的证据更为有限，但它也可能在人类乳腺癌中起因果作用。