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高毒力单纯疱疹病毒株经牙龈途径感染小鼠后不会导致小鼠死亡。

Highly virulent strains of herpes simplex virus fail to kill mice following infection via gingival route.

作者信息

Monma Y, Chen Z J, Mayama H, Kamiyama K, Shimizu F

机构信息

Department of Pediatric Dentistry, Tohoku University School of Dentistry, Sendai, Japan.

出版信息

J Dent Res. 1996 Apr;75(4):974-9. doi: 10.1177/00220345960750041201.

DOI:10.1177/00220345960750041201
PMID:8708138
Abstract

Virulence of herpes simplex virus (HSV) in mice has been demonstrated to be dependent on the site of infection. In this experiment, pathogenesis of HSV was studied in 2 different routes of infection in a mouse model system. When BALB/c mice were infected with 5 x 10(3) plaque-forming units (PFU) of virulent HSV type 1 Miyama GC+ strain (HSV-1-GC+) intraperitoneally, all mice were dead in 6 to 9 days. HSV-1-GC+ was recovered from organs such as the cerebrum, cerebellum, brainstem, and spleen 2 to 5 days after infection, but not from other organs such as trigeminal ganglia. However, if mice were infected in the maxillary gingiva with 1.0 x 10(7) PFU of HSV-1-GC+, all mice survived. HSV-1-GC+ was recovered from the trigeminal ganglia and brainstem 2 to 5 days after infection, but not from other organs tested. When mice were infected in maxillary gingiva with HSV-1-GC+, followed by the intraperitoneal injection of 6 mg of cyclophosphamide 72 hrs after virus infection, all mice were dead within days. Immunofluorescent and hematoxylin-eosin staining of gingival tissue sections revealed that when mice were infected in maxillary gingiva with HSV-1-GC+, 3 times as many gamma delta T-cells and 5 times as many polymorphonuclear cells can be detected in sections of maxillary gingiva when compared with non-infected mice. These data show that the gingiva of mice is considerably more resistant to infection with HSV, compared with the peritoneal cavity, and suggest the possible presence of an oral defense mechanism which might be different from that in the peritoneal cavity.

摘要

单纯疱疹病毒(HSV)在小鼠中的毒力已被证明取决于感染部位。在本实验中,在小鼠模型系统中研究了HSV在两种不同感染途径下的发病机制。当用5×10³空斑形成单位(PFU)的强毒1型宫山GC⁺株单纯疱疹病毒(HSV-1-GC⁺)腹腔感染BALB/c小鼠时,所有小鼠在6至9天内死亡。感染后2至5天,可从大脑、小脑、脑干和脾脏等器官中分离出HSV-1-GC⁺,但从三叉神经节等其他器官中未分离到。然而,如果用1.0×10⁷ PFU的HSV-1-GC⁺在上颌牙龈感染小鼠,所有小鼠均存活。感染后2至5天,可从三叉神经节和脑干中分离出HSV-1-GC⁺,但在所检测的其他器官中未分离到。当小鼠在上颌牙龈感染HSV-1-GC⁺,并在病毒感染72小时后腹腔注射6毫克环磷酰胺时,所有小鼠在数天内死亡。牙龈组织切片的免疫荧光和苏木精-伊红染色显示,当小鼠在上颌牙龈感染HSV-1-GC⁺时,与未感染小鼠相比,上颌牙龈切片中可检测到的γδT细胞数量是其3倍,多形核细胞数量是其5倍。这些数据表明,与腹腔相比,小鼠牙龈对HSV感染的抵抗力要强得多,并提示可能存在一种不同于腹腔的口腔防御机制。

相似文献

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Highly virulent strains of herpes simplex virus fail to kill mice following infection via gingival route.高毒力单纯疱疹病毒株经牙龈途径感染小鼠后不会导致小鼠死亡。
J Dent Res. 1996 Apr;75(4):974-9. doi: 10.1177/00220345960750041201.
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Interleukin-12- and gamma interferon-dependent innate immunity are essential and sufficient for long-term survival of passively immunized mice infected with herpes simplex virus type 1.白细胞介素-12和γ干扰素依赖性天然免疫对于被动免疫的感染1型单纯疱疹病毒小鼠的长期存活至关重要且足够。
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Herpes simplex virus type 1 (HSV-1) UL56 gene is involved in viral intraperitoneal pathogenicity to immunocompetent mice.单纯疱疹病毒1型(HSV-1)UL56基因与病毒对免疫活性小鼠的腹腔致病性有关。
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Recombinant herpes simplex virus type 1 expressing murine interleukin-4 is less virulent than wild-type virus in mice.表达小鼠白细胞介素-4的重组1型单纯疱疹病毒在小鼠中的毒性低于野生型病毒。
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The UL55 and UL56 genes of herpes simplex virus type 1 are not required for viral replication, intraperitoneal virulence, or establishment of latency in mice.单纯疱疹病毒1型的UL55和UL56基因对于病毒复制、腹腔内毒力或在小鼠中建立潜伏感染并非必需。
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Herpes simplex type 1 infects and establishes latency in the brain and trigeminal ganglia during primary infection of the lip in cotton rats and mice.在棉鼠和小鼠的唇部初次感染期间,单纯疱疹病毒1型会感染大脑和三叉神经节并在其中建立潜伏感染。
Arch Virol. 2002;147(1):167-79. doi: 10.1007/s705-002-8309-9.

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