Thind I S, Singh N P
Acta Virol. 1977 Jul;21(4):317-25.
Pathogenesis was studied in mice with moderate levels of lead intoxication after Langat virus infection. Both lead chloride and lead nitrate increased mortality by 40--50%. This increase was associated with decreased in vivo interferon and neutralizing antibody synthesis. The increased mortality was associated with enhancement of viral growth in peripheral tissues as evidenced by early appearing and long-lasting high titer viremia following lead intoxication. This resulted in early penetration of blood brain barrier and led to much higher virus titers in the brain. The data strongly suggest that lead increased mortality following infection by complex means, the most important being the enhacement of encephalitogenic potential of Langat virus.
在感染兰加特病毒后，对处于中度铅中毒水平的小鼠的发病机制进行了研究。氯化铅和硝酸铅均使死亡率增加了40%至50%。这种增加与体内干扰素和中和抗体合成减少有关。死亡率的增加与外周组织中病毒生长的增强有关，铅中毒后早期出现且持久的高滴度病毒血症证明了这一点。这导致血脑屏障早期被穿透，并使大脑中的病毒滴度高得多。数据有力地表明，铅通过复杂的方式增加感染后的死亡率，其中最重要的是增强了兰加特病毒的致脑炎潜力。
