Syphilis superinfection activates expression of human immunodeficiency virus I in latently infected rabbits

Chien-Te Tseng, M. A. Hughes, P. L. Hsu, S. Mahoney, M. Duvic, S. Sell

Research output: Contribution to journalArticle

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Abstract

Superinfection of latently human immunodeficiency virus (HIV)-infected rabbits with either Treponema pallidum or Shope fibroma virus (SFV) activates HIV expression. In addition, HIV-infected rabbits demonstrate prolonged cutaneous lesions (chancres) after intracutaneous challenge with T. pallidum, the causative agent of syphilis. Rabbits were infected by intravenous inoculation of 3 X 107 human T-cell lymphotrophic virus type III (HTLV-III)/B10 (HIV-1)- infected H9 (human) cells. Five weeks after initial infection, integrated HIV-1 - specific DNA sequences were detected in the DNA of the peripheral blood lymphocytes of only one of eight rabbits using polymerase chain reactions (PCR); human DNA could not be detected at this time. Furthermore HIV infection could not be demonstrated by either seroconversion or PCR during the next 6 months. All HIV-infected rabbits remained clinically healthy and had normal white blood cell counts. Six months after HIV infection, four HIV-infected and two noninfected controls were superinfected with 106 T. pallidum in eight skin sites in the shaved skin of the back, and four infected and two control animals were challenged with an intradermal injection with SFV. After infection with either syphilis or SFV, the DNA from the white blood cells of all eight HIV-infected rabbits contained HIV sequences, and HIV sequences were demonstrated in dermal mononuclear cells of the syphilitic lesions by in situ hybridization. The SFV-induced tumors were rejected normally in the HIV-infected rabbits, but four of the four rabbits challenged with T. pallidum had delayed development of cutaneous lesions and three of four demonstrated larger and more prolonged lesions. White blood counts, mitogen responses, and interleukin-2 production remained within normal limits, and seroconversion for HIV was not detected. Three of four rabbits in a second group, challenged with T. pallidum 4 months after HIV-inoculation, also had delayed healing of syphilitic lesions. These results indicate that latent HIV-infection of rabbits may be activated by immunostimulation and that latently HIV-infected rabbits have impaired delayed hypersensitivity reactions. It is hypothesized that true latent HIV- infection in the rabbits is in monocytes and postulated that further immunostimulation may produce infection of lymphocytes and activation of disease.

Original languageEnglish (US)
Pages (from-to)1149-1164
Number of pages16
JournalAmerican Journal of Pathology
Volume138
Issue number5
StatePublished - May 1991
Externally publishedYes

Fingerprint

Superinfection
Syphilis
HIV
Rabbits
Rabbit Fibroma Virus
Treponema pallidum
Virus Diseases
Skin
HIV-1
Immunization
DNA
Chancre
Infection
Intradermal Injections
Polymerase Chain Reaction
Delayed Hypersensitivity
Lymphocyte Activation

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

Cite this

Syphilis superinfection activates expression of human immunodeficiency virus I in latently infected rabbits. / Tseng, Chien-Te; Hughes, M. A.; Hsu, P. L.; Mahoney, S.; Duvic, M.; Sell, S.

In: American Journal of Pathology, Vol. 138, No. 5, 05.1991, p. 1149-1164.

Research output: Contribution to journalArticle

Tseng, Chien-Te ; Hughes, M. A. ; Hsu, P. L. ; Mahoney, S. ; Duvic, M. ; Sell, S. / Syphilis superinfection activates expression of human immunodeficiency virus I in latently infected rabbits. In: American Journal of Pathology. 1991 ; Vol. 138, No. 5. pp. 1149-1164.
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abstract = "Superinfection of latently human immunodeficiency virus (HIV)-infected rabbits with either Treponema pallidum or Shope fibroma virus (SFV) activates HIV expression. In addition, HIV-infected rabbits demonstrate prolonged cutaneous lesions (chancres) after intracutaneous challenge with T. pallidum, the causative agent of syphilis. Rabbits were infected by intravenous inoculation of 3 X 107 human T-cell lymphotrophic virus type III (HTLV-III)/B10 (HIV-1)- infected H9 (human) cells. Five weeks after initial infection, integrated HIV-1 - specific DNA sequences were detected in the DNA of the peripheral blood lymphocytes of only one of eight rabbits using polymerase chain reactions (PCR); human DNA could not be detected at this time. Furthermore HIV infection could not be demonstrated by either seroconversion or PCR during the next 6 months. All HIV-infected rabbits remained clinically healthy and had normal white blood cell counts. Six months after HIV infection, four HIV-infected and two noninfected controls were superinfected with 106 T. pallidum in eight skin sites in the shaved skin of the back, and four infected and two control animals were challenged with an intradermal injection with SFV. After infection with either syphilis or SFV, the DNA from the white blood cells of all eight HIV-infected rabbits contained HIV sequences, and HIV sequences were demonstrated in dermal mononuclear cells of the syphilitic lesions by in situ hybridization. The SFV-induced tumors were rejected normally in the HIV-infected rabbits, but four of the four rabbits challenged with T. pallidum had delayed development of cutaneous lesions and three of four demonstrated larger and more prolonged lesions. White blood counts, mitogen responses, and interleukin-2 production remained within normal limits, and seroconversion for HIV was not detected. Three of four rabbits in a second group, challenged with T. pallidum 4 months after HIV-inoculation, also had delayed healing of syphilitic lesions. These results indicate that latent HIV-infection of rabbits may be activated by immunostimulation and that latently HIV-infected rabbits have impaired delayed hypersensitivity reactions. It is hypothesized that true latent HIV- infection in the rabbits is in monocytes and postulated that further immunostimulation may produce infection of lymphocytes and activation of disease.",
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