Zanin Mark, Koçer Zeynep A, Poulson Rebecca L, Gabbard Jon D, Howerth Elizabeth W, Jones Cheryl A, Friedman Kimberly, Seiler Jon, Danner Angela, Kercher Lisa, McBride Ryan, Paulson James C, Wentworth David E, Krauss Scott, Tompkins Stephen M, Stallknecht David E, Webster Robert G
Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
Department of Population Health, University of Georgia, Athens, Georgia, USA.
J Virol. 2017 Jan 18;91(3). doi: 10.1128/JVI.01934-16. Print 2017 Feb 1.
H7 subtype influenza A viruses are widely distributed and have been responsible for human infections and numerous outbreaks in poultry with significant impact. Despite this, the disease-causing potential of the precursor low-pathogenic (LP) H7 viruses from the wild bird reservoir has not been investigated. Our objective was to assess the disease-causing potential of 30 LP H7 viruses isolated from wild avian species in the United States and Canada using the DBA/2J mouse model. Without prior mammalian adaptation, the majority of viruses, 27 (90%), caused mortality in mice. Of these, 17 (56.7%) caused 100% mortality and 24 were of pathogenicity similar to that of A/Anhui/1/2013 (H7N9), which is highly pathogenic in mice. Viruses of duck origin were more pathogenic than those of shorebird origin, as 13 of 18 (72.2%) duck origin viruses caused 100% mortality while 4 of 12 (33.3%) shorebird origin viruses caused 100% mortality, despite there being no difference in mean lung viral titers between the groups. Replication beyond the respiratory tract was also evident, particularly in the heart and brain. Of the 16 viruses studied for fecal shedding, 11 were detected in fecal samples. These viruses exhibited a strong preference for avian-type α2,3-linked sialic acids; however, binding to mammalian-type α2,6-linked sialic acids was also detected. These findings indicate that LP avian H7 influenza A viruses are able to infect and cause disease in mammals without prior adaptation and therefore pose a potential public health risk.
Low-pathogenic (LP) avian H7 influenza A viruses are widely distributed in the avian reservoir and are the precursors of numerous outbreaks of highly pathogenic avian influenza viruses in commercial poultry farms. However, unlike highly pathogenic H7 viruses, the disease-causing potential of LP H7 viruses from the wild bird reservoir has not been investigated. To address this, we studied 30 LP avian H7 viruses isolated from wild avian species in the United States and Canada using the DBA/2J mouse model. Surprisingly, the majority of these viruses, 90%, caused mortality in mice without prior mammalian adaptation, and 56.7% caused 100% mortality. There was also evidence of spread beyond the respiratory tract and fecal shedding. Therefore, the disease-causing potential of LP avian H7 influenza A viruses in mammals may be underestimated, and these viruses therefore pose a potential public health risk.
H7亚型甲型流感病毒广泛分布，已导致人类感染以及家禽中多次爆发疫情，造成重大影响。尽管如此，来自野生鸟类宿主的低致病性（LP）H7病毒的致病潜力尚未得到研究。我们的目标是使用DBA/2J小鼠模型评估从美国和加拿大的野生鸟类物种中分离出的30株LP H7病毒的致病潜力。在未经事先适应哺乳动物的情况下，大多数病毒，即27株（90%），导致小鼠死亡。其中，17株（56.7%）导致100%的死亡率，24株的致病性与A/安徽/1/2013（H7N9）相似，后者对小鼠具有高致病性。鸭源病毒比滨鸟源病毒更具致病性，18株鸭源病毒中有13株（72.2%）导致100%的死亡率，而12株滨鸟源病毒中有4株（33.3%）导致100%的死亡率，尽管两组之间的平均肺病毒滴度没有差异。呼吸道以外的复制也很明显，特别是在心脏和大脑中。在研究的16株病毒的粪便排毒情况中，有11株在粪便样本中被检测到。这些病毒对禽源α2,3连接的唾液酸表现出强烈偏好；然而，也检测到它们与哺乳动物源α2,6连接的唾液酸结合。这些发现表明，LP禽源H7甲型流感病毒无需事先适应就能感染哺乳动物并导致疾病，因此构成潜在的公共卫生风险。
低致病性（LP）禽源H7甲型流感病毒广泛分布于鸟类宿主中，是商业家禽养殖场中多次高致病性禽流感病毒爆发的前身。然而，与高致病性H7病毒不同，来自野生鸟类宿主的LP H7病毒的致病潜力尚未得到研究。为了解决这个问题，我们使用DBA/2J小鼠模型研究了从美国和加拿大的野生鸟类物种中分离出的30株LP禽源H7病毒。令人惊讶的是，这些病毒中的大多数，即90%，在未经事先适应哺乳动物的情况下导致小鼠死亡，56.7%导致100%的死亡率。也有证据表明病毒在呼吸道以外传播并通过粪便排毒。因此，LP禽源H7甲型流感病毒在哺乳动物中的致病潜力可能被低估，这些病毒因此构成潜在的公共卫生风险。
