Comparative pathogenicity of type 1 and type 2 isolates of porcine reproductive and respiratory syndrome virus (PRRSV) in a young pig infection model

生物 猪繁殖与呼吸综合征病毒 基因型 病毒 呼吸系统 病毒学 致病性 病毒载量 兽医学 毒力 微生物学 内科学 基因 医学 遗传学 解剖
作者
Francisco Javier Martínez-Lobo,Francisco Díez‐Fuertes,Joaquím Segalés,Carlos Garcı́a-Artiga,I. Simarro,J. M. Castro,Marta Cerezo Prieto
出处
期刊:Veterinary Microbiology [Elsevier BV]
卷期号:154 (1-2): 58-68 被引量:80
标识
DOI:10.1016/j.vetmic.2011.06.025
摘要

Porcine reproductive and respiratory syndrome virus (PRRSV) isolates are classified in two different genotypes, based on genomic heterogeneity: type 1, which comprises European type isolates, and type 2, which includes North American type isolates. It is believed that members of both genotypes differ in some biological properties including pathogenicity, however extensive studies comparing isolates of both genotypes have never been carried out. The objective of the present study was to compare the pathogenic properties of six different PRRSV isolates, three of type 1 and three of type 2, in a young pig infection model. For this purpose, a total of 105 3-week-old piglets were divided in 7 groups of 15 animals that were exposed on day 0 of the experiment to one of the six isolates tested or were mock infected (negative control group). Clinical signs and rectal temperatures were recorded daily and blood samples were taken on days 3, 6, 9, 12, 15, 18 and 21 of the experiment. On days 7, 14 and 21 post-inoculation five animals per group were sacrificed, macroscopic lung lesions were evaluated and different tissue samples were collected to determine viral organic distribution. The results obtained indicate that type 2 isolates are more pneumovirulent than type 1 isolates, as demonstrated by the recording of respiratory clinical signs only in pigs exposed to type 2 viruses and by the severity of macroscopic and microscopic lung lesions in those pigs. However, no clear differences could be established between genotypes in systemic clinical signs or viral load and viral distribution after challenge. These results support the general idea that type 2 isolates induce more severe respiratory disease than type 1 isolates.
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