多种病毒与乳腺癌有关，包括人疱疹病毒 4 (HHV4)、人疱疹病毒 5 (HHV5)、人乳头瘤病毒 (HPV)、人 JC 多瘤病毒 (JCV)、人内源性逆转录病毒 K 组 (HERVK)、牛白血病病毒（BLV）和小鼠乳腺肿瘤病毒（MMTV）。人类白细胞抗原 (HLA) 参与病毒消除，并已被证明会影响乳腺癌的保护/易感性。在这里，我们研究了这样一个假设：病毒对乳腺癌发展的贡献取决于病毒的存在，而病毒的存在又与消除病毒的成功成反比。为此，我们通过计算机估计了上述 7 种病毒的蛋白质与 127 个常见 HLA 等位基因（69 个 I 类 [HLA-I] 和 58 个 II 类 HLA-II]）的预测结合亲和力 (PBA)，并研究了这些基因之间的关联与相同等位基因的乳腺癌-HLA (BC-HLA) 免疫遗传学谱的结合亲和力。使用层次树聚类，我们发现，对于 HLA-I，病毒 BLV、JCV 和 MMTV 与 BC-HLA 分组，而对于 HLA-II，病毒 BLV、HERVK、HPV、JCV 和 MMTV 与 BC 分组-HLA。最后，对于两个 HLA 类别，与 BC-HLA 谱分组的病毒的平均 PBA 显着低于其他非 BC-HLA 相关病毒的平均 PBA。假设低 PBA 可能与较慢的病毒消除有关，这些发现支持这样的假设：有缺陷/较慢的消除，因此，针对它们的抗体的持久性较长和低效/延迟产生是观察到的低 PBA 组与乳腺癌之间的关联的基础。 cancer.© 2024。这是美国政府的作品，在美国不受版权保护；外国版权保护可能适用。

Several viruses have been implicated in breast cancer, including human herpes virus 4 (HHV4), human herpes virus 5 (HHV5), human papilloma virus (HPV), human JC polyoma virus (JCV), human endogenous retrovirus group K (HERVK), bovine leukemia virus (BLV) and mouse mammary tumor virus (MMTV). Human leukocyte antigen (HLA) is involved in virus elimination and has been shown to influence breast cancer protection/susceptibility. Here we investigated the hypothesis that the contribution of a virus to development of breast cancer would depend on the presence of the virus, which, in turn, would be inversely related to the success of its elimination. For that purpose, we estimated in silico predicted binding affinities (PBA) of proteins of the 7 viruses above to 127 common HLA alleles (69 Class I [HLA-I] and 58 Class II HLA-II]) and investigated the association of these binding affinities to the breast cancer-HLA (BC-HLA) immunogenetic profile of the same alleles. Using hierarchical tree clustering, we found that, for HLA-I, viruses BLV, JCV and MMTV were grouped with the BC-HLA, whereas, for HLA-II, viruses BLV, HERVK, HPV, JCV, and MMTV were grouped with BC-HLA. Finally, for both HLA classes, the average PBAs of the viruses grouped with the BC-HLA profile were significantly lower than those of the other, non BC-HLA associated viruses. Assuming that low PBAs are likely associated with slower viral elimination, these findings support the hypothesis that a defective/slower elimination and, hence, longer persistence and inefficient/delayed production of antibodies against them underlies the observed association of the low-PBA group with breast cancer.© 2024. This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply.