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甲型流感病毒７５－３９株鼠肺适应型经鼻腔感染小鼠，可使小鼠致病并发生死亡，ＬＤ５０为３．６７。而经皮下和腹腔感染无致病性，存活率１００％。基于经腹腔注射无致病性的实验结果，进而用此病毒治疗Ｓ＿（３７）腹水瘤小鼠，存活率达９３．３％。体外流感病毒感染Ｓ＿（３７）肿瘤细胞，经不同时间观测，至第３天时Ｓ＿（３７）细胞经台盼蓝染色，发现细胞１００％死亡，而对照组Ｓ＿（３７）细胞死亡率为１０％左右（Ｐ＜０．０１）。进一步研究病毒免疫治疗Ｓ＿（３７）腹水瘤小鼠的机理，发现经病毒感染后小鼠ＮＫ细胞杀伤活性升高达５８％，正常小鼠ＮＫ活性为２２％，两者有显著性差异（Ｐ＜０．０１）。同时，检测注射病毒后小鼠腹腔巨噬细胞的吞噬活性也随之升高。
Influenza A virus 75-39 strains of mice adapted to infection of the nasal cavity in mice can cause disease and death in mice with an LD50 of 3.67. Subcutaneous and intra-abdominal infections were non-pathogenic and the survival rate was 100%. Based on the experimental results of no pathogenicity by intraperitoneal injection, the survival rate of the mice with S_(37) ascites tumor was 93.3%. In vitro influenza virus infected S_(37) tumor cells were observed at different times. On the third day, S_(37) cells were stained with trypan blue and 100% cells were found to be dead, whereas the control group had S_(37) cell death rate of 10%. Left and right (P<0.01). Further study of the mechanism of viral immunotherapy for S_(37) ascites tumor mice revealed that the killing activity of mouse NK cells after viral infection was up to 58%, and the NK activity of normal mice was 22%, there was a significant difference between them (P< 0.01). At the same time, the phagocytic activity of mouse peritoneal macrophages after injection of virus was also increased.