Segovia J C, Bueren J A, Almendral J M
Centro de Investigaciones Energéticas Medioambientales y Tecnológicas (CIEMAT), Madrid, Spain.
J Virol. 1995 May;69(5):3229-32. doi: 10.1128/JVI.69.5.3229-3232.1995.
The in vivo myelosuppressive capacity of strain i of the parovirus minute virus of mice (MVMi) was investigated in newborn BALB/c mice inoculated with a lethal intranasal dose. MVMi infection reached maximum levels of DNA synthesis and infectious titers in lymphohemopoietic organs at 4 to 6 days postinoculation and was restricted by an early neutralizing humoral immune response. After viral control (by 10 days postinoculation), a significant decrease in femoral and splenic cellularity, as well as in granulocyte-macrophage colony-forming unit and erythroid burst-forming unit hemopoietic progenitors, was observed in most inoculated animals. This delayed myeloid depression, although it may be not a major cause of the lethality of the infection, implies indirect pathogenic mechanisms induced by MVMi infection in a susceptible host.
在用致死性鼻内剂量接种的新生BALB/c小鼠中,研究了小鼠细小病毒i株(MVMi)的体内骨髓抑制能力。接种后4至6天,MVMi感染在淋巴造血器官中达到DNA合成和感染滴度的最高水平,并受到早期中和体液免疫反应的限制。病毒得到控制后(接种后10天),在大多数接种动物中观察到股骨和脾脏细胞数量显著减少,以及粒细胞-巨噬细胞集落形成单位和红系爆式集落形成单位造血祖细胞数量减少。这种延迟性骨髓抑制,尽管可能不是感染致死的主要原因,但意味着MVMi感染在易感宿主中诱导了间接致病机制。