Herpes Simplex Keratitls in Patients with Acquired Immune Deficlency Syndrome

Young, Terri L.; Robin, Jeffrey B.; Holland, Gary N.; Hendricks, Robert L.; Paschal, John F.; Engstrom, Robert E.; Sugar, Joel

doi:10.1016/s0161-6420(89)32706-0

Cited by 53 publications

(20 citation statements)

References 11 publications

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“…HSV infection can in some cases spread beyond the sensory neurons to produce a disseminated infection. This is particularly the case in neonates or immunocompromised individuals, such as AIDS patients or organ transplant recipients, where multiorgan involvement or infection of the CNS can lead to high mortality (2)(3)(4)(5)(6)(7)(8)(9). In various studies, the presence of anti-HSV-1 serum Ab has been shown to protect against complications of HSV infection, presumably through limiting systemic viral spread (10 -12).…”

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confidence: 99%

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Cutting Edge: Myeloid Complement C3 Enhances the Humoral Response To Peripheral Viral Infection

Verschoor

Brockman

Knipe

et al. 2001

The Journal of Immunology

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HSV-1 is the causative agent of cutaneous lesions, commonly referred to as cold sores. Primary exposure to the virus ordinarily occurs through the periphery, in particular through abraded skin or mucosal membranes. Under certain circumstances (e.g., in neonatals or AIDS patients), the infection becomes disseminated, often with severe consequences. Spread of HSV-1 is limited by virus-specific Ab. The development of an efficient humoral response to the virus is dependent on innate immunity component complement C3. The liver is the major source of C3, but there are also extrahepatic origins of C3 such as lymphoid macrophages. In the present study, the significance of C3 synthesis by bone marrow-derived cells was assessed by the transfer of wild-type bone marrow into irradiated C3-deficient mice. Using these chimeric mice, extrahepatic C3 was determined sufficient to initiate specific Ab and memory responses to a peripheral HSV-1 infection.

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confidence: 99%

“…Humoral responses to HSV-1 are thymus-dependent (TD) 3 ; Th cells are required to provide a costimulatory signal to activate B cells. Cytokine profiles and IgG isotype patterns indicate that T lymphocyte help in HSV-1 infection is skewed toward Th-1 (17,18).…”

mentioning

confidence: 99%

Cutting Edge: Myeloid Complement C3 Enhances the Humoral Response To Peripheral Viral Infection

Verschoor

Brockman

Knipe

et al. 2001

The Journal of Immunology

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“…The limited literature on immunosuppression and ocular herpetic infections in humans suggests HSK as an important problem to be monitored during renal transplantation [14, 15, 16]since that had a rapid clinical course and took prolonged acyclovir therapy to heal. An effect of the HIV status on HSK is also reported [17, 18], even though it has not been studied in detail.…”

Section: Discussionmentioning

confidence: 99%

Influence of Human Immunodeficiency Virus Status on the Clinical History of Herpes simplex Keratitis

et al. 2000

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Human immunodeficiency virus (HIV) infection is associated with a wide spectrum of systemic and ocular infectious diseases. Little is known about its association with herpes simplex keratitis (HSK) in this geographical region (South India). A retrospective study was undertaken to analyze this association in a cohort of 30 virologically proven recurrent HSK cases. Laboratory methods included herpes simplex virus (HSV) isolation, HSV antigen detection and tear secretory IgA or HSV DNA detection while commercial ELISA kits detected HIV infection. The rationale behind the HIV screening was to assess the role of HIV with increased HSK recurrences. Confirmed HIV seropositivity was 16.7% in recurrent HSK cases as against 3.3% in the matched first-episode HSK cases (p < 0.05, Fisher’s exact test). Our observations on the features of herpetic keratitis in HIV-proven patients, though based on a small number of cases, raise the question whether the immunological abnormalities associated with HIV/AIDS may affect the clinical course of HSK.

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“…There may be more predilection for marginal rather than central ulcers, epithelial keratitis, resistance to treatment and more frequent and lengthier recurrences. 24 The recurrence rate is nearly 2.5 times more frequent than immunocompetent hosts. The T lymphocyte deficiency may actually prevent this group of patients from stromal disease.…”

Section: Hsvmentioning

confidence: 99%