Advertisement

Chinese Journal of Cancer Research

, Volume 6, Issue 4, pp 241–247 | Cite as

The cervix multi-viruses infection and the development of cervical carcinomas

  • Zhang Wei 
  • Jin Shunqian 
  • Liu Boqi 
  • Liang Xiao 
  • Ming Lihua 
  • Wang Xiaohong 
  • Shang Ming 
  • Sun Jianheng
  • Wang Xixia
  • Zhang Wenhua
  • Wu Airu
  • Liu Chiming
  • Li Junyao
Basic Investigations
  • 13 Downloads

Abstract

The infections of human papilloma virus (HPV), herpes simplex virus type 2 (HSV-2) and Epstein-Barr virus (EBV) to human cervical epithelium are universal and some of them are associated with the development of cervical carcinomas. One hundred and eleven cervical cancer biopsies taken from Beijing area and Xiangyuan county in Shanxi province of China were examined for the presence of DNA sequences of HPV, HSV-2 and EBV by means of Dot blot hybridization. The experiment results showed that the total infectious rates of HPV, HSV-2 and EBV were 71.17% (79/111), 14.44% (16/111) and 15.63% (15/96), respectively. Seventy-nine samples positive for HPV were further analysed for the viral types distribution, the result indicated that the positive specimens of HPV type 16 accounted for 72.15%; otherwise, the biopsies positive for HPV type 18 and 6B/11 only accounted for 16.46% and 11.39%, respectively. The data suggested that HPV infection, especially HPV type 16, may play an important role in the development of cervical carcinomas. 16 specimens positive for HSV-2 were examined for HPV DNA sequences and the result uncovered that 13 out of them were HPV16 positive (81.25%); 11 samples containing EBV genomes were also examined for HPV DNA sequences and the result indicated that 9 of 11 were detectable for HPV DNA. The experiment results proved a direct evidence of multi-virus infection in cervix and of the synergistic interaction among viruses in the process of cervical epithelial carcinogenesis. Comparing of the viruses’ infection of two areas, the frequencies of HPV infection in Beijing and Xiangyuan areas were 72.84% (59/ 81) and 66.67% (20/30) ; the infectious rates of HSV-2 in the two areas were 8.64% (7/81) and 30% (9/30) (P<0.05); the rates of EBV infection in the two areas were 12.5% (10/80) and 31.25% (5/16) (0.1>P>0.05). The results proved another strong evidence that the high incidence of cervical cancer in Xiangyuan county may be closely correlated with multi-viruses infection and with multi-virus synergistic interaction.

Key words

Human papilloma virus (HPV) Cervical carcinomas Herpes simplex virus type 2 (HSV-2) Epstein-Barr Virus (EBV) 

References

  1. 1.
    Geo Von Krogh, Eva Rylander. Genitoanal papilloma virus infection. 1989; Karlstad, Sweden.Google Scholar
  2. 2.
    Rotkin ID. A comparison review of key epidemio-logical studies of cervical cancer related to current searches for transmissible agents. Cancer Res, 1973; 33: 1353.PubMedGoogle Scholar
  3. 3.
    Schneider A, Kraus H, Schuhmann IL et al. Papilloma-virous infection of the lower genital tract: Detection of viral DNA in gynecological swabs. Int J Cancer, 1985; 35: 443.PubMedCrossRefGoogle Scholar
  4. 4.
    Bedell MA, Jones KH, Laimins LA. The E6-E7 region of human papillomavirus type 18 is sufficient for transformation of NIII3T3 and Rat-1 cells. J Virol, 1987; 61: 3635.PubMedGoogle Scholar
  5. 5.
    Crook T, Morgenstern JP, Crawford L, et al. Continued expression of HPV 16 E7 proteins is required for maintenencr of the transformed phenotype of cells cotransformed by HPV 16 plus EJ-ras. EMBO J, 1989; 8: 513.PubMedGoogle Scholar
  6. 6.
    Palmer AE, London WT, Nahmias AJ, et al. A preliminary report on investigation of oncogenic potential of herpes simplex virus type 2 in cebus monkeys. Cancer Research 1976; 36: 807.PubMedGoogle Scholar
  7. 7.
    James P, Dyson N, Guide P, et al. Papillomavirus trans-activator protein E2 activates expression from the promoter for the ribonucleotide reductase large subunit from HSV-2. J General Virol. 1990; 71: 1817.CrossRefGoogle Scholar
  8. 8.
    Epstein MA. The Epstein-Barrr virus: Infection and tumour induction. Nature, 1986; 321: 653.PubMedCrossRefGoogle Scholar
  9. 9.
    Sixbey J W, Davis DS, Young LS, et al. Human epithelial cell expression of an EBV receptor. J General virol. 1987; 68: 805.CrossRefGoogle Scholar
  10. 10.
    Saemundsen AK, Albeck H, Hansen JPH, et al. Epstein-Barr virus in nasopharygeal and salivary gland carcinomas of Greeland Eskimoes. Bri J cancer. 1982; 46: 721.Google Scholar
  11. 11.
    Sixbey J W, Lemon SM, Pagano JS. A second site for EBV shedding: the uterin cervix. Lancet 1986; II(8516): 1122.CrossRefGoogle Scholar
  12. 12.
    Bevan I S, Blomafield PJ, Johnson MA, et al. Oncogenic viruses and cervical cancer. Lancet, 1989; 1(8643): 907.PubMedCrossRefGoogle Scholar

Copyright information

© Chinese Journal Of Cancer Research 1994

Authors and Affiliations

  • Zhang Wei 
    • 1
  • Jin Shunqian 
    • 1
  • Liu Boqi 
    • 1
  • Liang Xiao 
    • 1
  • Ming Lihua 
    • 1
  • Wang Xiaohong 
    • 1
  • Shang Ming 
    • 1
  • Sun Jianheng
    • 1
  • Wang Xixia
    • 1
  • Zhang Wenhua
    • 1
  • Wu Airu
    • 1
  • Liu Chiming
    • 1
  • Li Junyao
    • 1
  1. 1.Cancer Institute and HospitalCAMS and PUMCBeijing

Personalised recommendations