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单纯疮疹病毒Ｉ型（ＨＳＶ－Ｉ）属疱疹病毒科，它可引起人和动物的急性感染与持续性感染。国外文献报道，在ＨＳＶ－Ｉ感染的康复过程中，细胞免疫起着关键的作用。国内此类报道甚少。研究结果表明：ＨＳＶ－Ｉ标准株（ｋｏｓ）经自行扩增后，测得病毒毒力３．２×１０￣８ＴＣＩＤ５０／ｍｌ，ＬＤ５０为３．２８．并以１０￣４ＰＦＵ，ＨＳＶ－Ｉ经腹腔感染小鼠，建立感染动物模型。同时，用此病毒体外感染Ｐ８１５细胞，可在细胞表面检出ＨＳＶ－Ｉ病毒抗原。当小鼠感染ＨＳＶ－Ｉ病毒后，在感染初期脾细胞诱生ＩＦＮ的能力迅速上升（感染鼠２５６．０±０．０Ｕ／ｍｌ，正常鼠３７．３±６．０Ｕ／ｍｌ），至２１天时降至正常组水平，这一变化与感染鼠ＮＫ活性动态观察结果相吻合。实验还发现，ＨＳＶ－Ｉ感染鼠脾细胞诱生ＩＬ－２的能力也是增高的。虽然在感染早期有一短暂的下降，这可能与动物在感染初期的应激状态有关。结合体外诱导ＬＡＫ及ＨＳＶ－Ｉ／ＣＴＬ实验结果推测，脾细胞诱生细胞因子能力的增高，为体内产生ＬＡＫ及ＣＴＬ提供了条件。体内转移试验进一步证实ＬＡＫ及ＨＳＶ－Ｉ／ＣＴＬ在体内对感染鼠均有不同程度的保护作用，以过继转移ＨＳＶ－Ｉ／ＣＴＬ的保护作用更强。
Herpes Simplex Virus Type 1 (HSV-I) is a herpes simplex virus that causes acute and persistent infections in humans and animals. Foreign literature reports that in the process of HSV-I infection, cellular immunity plays a key role. Domestic such reports rarely. The results showed that the virus virulence of HSV-I strain (kos) was 3.2 × 10 ~ 8 TCID50 / ml and LD50 was 3.28 after self-amplification. Infected with 10 ~ 4PFU, HSV-I by intraperitoneal infection in mice. At the same time, in vitro infection of P815 cells with this virus can detect HSV-I viral antigens on the cell surface. When mice were infected with HSV-I virus, the ability of splenocytes to induce IFN was rapidly increased (256.0 ± 0.0U / ml in infected mice and 37.3 ± 6.0U / ml in normal mice) to 21 Day dropped to the normal group level, this change consistent with the dynamic observation of infected mice NK activity. The experiment also found that HSV-I infected mouse spleen cells induced IL-2 also increased. Although there is a brief drop in the early stages of infection, this may be related to the animal’s initial stress state. Combined with in vitro induction of LAK and HSV-I / CTL experimental results speculated that splenocytes induced cytokines increased capacity for the production of LAK and CTL provide the conditions. The in vivo transfer test further confirmed that LAK and HSV-I / CTL had protective effects in vivo to varying degrees in vivo, and that the protective effect of HSV-I / CTL was stronger than that of HSV-I / CTL.