腹泻是肇因于轮状病毒的多重活动。轮状病毒主要复制于消化道[29],并感染肠绒毛的肠细胞(英语:Enterocyte),造成上皮组织结构和功能上的改变[30],遭到该病毒的破坏而导致吸收不良。产生肠毒素的病毒蛋白质NSP4制造了倚赖钙离子的氯化分泌物,破坏了钠-葡萄糖协同运输蛋白1(sodium-glucose transport 1,SGLT1)载体[31]居中调节的水份再吸收,这个显然降低了刷状缘(brush border)薄膜双糖酵素(disaccharidase)的活动,而且可能激化肠神经系统中依赖钙离子的分泌(secretion)的反射作用[32][33]。健康的肠黏膜细胞会分泌乳糖酶进入小肠;所以因乳糖酶缺乏而造成的乳糖不耐症也是轮状病毒感染经常出现的症状[34][35],这个症状可以持续数周[36]。乳糖不耐症的再次发生通常与牛奶再次引入儿童的日常饮食有关,因为细菌发酵了在肚子内的双糖乳糖[37]。
轮状病毒疫苗计画(Rotavirus Vaccine Program)是一个适宜卫生科技组织(Program for Appropriate Technology in Health,简写为 PATH)、世界卫生组织与美国疾病控制与预防中心的合作计画,该计画由全球疫苗与免疫联盟(GAVI Alliance)资助。该计画的目的是借由制造可以让发展中国家使用的轮状病毒疫苗,来降低儿童因为痢疾而产生的疾病与儿童死亡率[80]。
1974年,汤玛斯·亨利·费留特(Thomas Henry Flewett)在通过电子显微镜观察过这类病毒之后,建议将其命名为“轮状病毒”(rotavirus),因为轮状病毒的颗粒看起来很像轮子,而拉丁文中“rota”的意思即为“轮状”[125][126];这个名称四年后经由国际病毒分类委员会(International Committee on Taxonomy of Viruses)正式认可[127]。1976年,相关类似的病毒也在许多其他种动物的研究上被描述到[123]。这些被报告描述的病毒,通通都会导致急性肠胃炎,并且被认定为影响全世界人类与动物的集体病原体[125]。轮状病毒的血清型于1980年首次发表[128],而在隔年,来自人体的轮状病毒借由添加胰蛋白酶(一种发现于哺乳动物十二指肠的酶,目前已知是轮状病毒复制所必须的物质)首次在从自然环境中猴子肾脏取得的细胞培养中成功栽培[129]。成功培养轮状病毒的能力加速了研究的脚步,且在1980年代中期,首批候选的疫苗已经开始进行评估[130]。
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