Severe cytomegalovirus pneumonitis in HIV infected patients with higher than average CD4 counts.

Squire, S. Bertel; Lipman, Marc; Bagdades, Evis; Mulvenna, P.; Grundy, J. E.; Griffiths, Paul; Ma, Jun

doi:10.1136/thx.47.4.301

Cited by 32 publications

(13 citation statements)

References 16 publications

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“…Thus, patients with AIDS who frequently harbour CMV in their lungs have a low incidence of CMV pneumonitis, 34 whereas the disease has been observed in HIV positive individuals with high CD4+ cell numbers. 35 The recent introduction of highly active antiretroviral therapy (HAART) for HIV infection has resulted in an inflammatory vitritis in patients with CMV retinitis which, in some cases, has resulted in the loss of vision. 36 37 Thus, paradoxically, the CMV replication accompanying sight threatening CMV retinitis can be controlled by the administration of HAART but the regeneration of specific immune responses causes a new pathology, which can be equally destructive to the host tissue and deleterious to the quality of life of the patient.…”

Section: Pathological Consequences Of CMV Infectionmentioning

confidence: 99%

Investigation of CMV disease in immunocompromised patients

Emery

2001

Journal of Clinical Pathology

129

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Cytomegalovirus (CMV) is a recognised cause of morbidity and mortality in immunocompromised individuals. This review will concentrate on recent advances in the understanding of the complex interplay between the host and parasite and the pathological consequences of perturbation of the host immune system. The classic view of CMV as a slowly replicating virus is challenged by recent in vivo findings suggesting that active replication occurs dynamically in the human host, with a doubling time of approximately one day. In addition, CMV load plays a major role in viral pathogenesis, such that increased CMV replication is a significant risk factor for disease in all immunocompromised groups studied to date. These studies focus attention on understanding the virological and immunological determinants of enhanced viral replication and its pathological consequences.

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Section: Pathological Consequences Of CMV Infectionmentioning

confidence: 99%

Investigation of CMV disease in immunocompromised patients

Emery

2001

Journal of Clinical Pathology

129

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“…These results again indicate that host factors, which are important in producing HCMV-related pathology, are absent or severely depleted in the HIVinfected patient group. Interestingly, HCMV DNA is frequently found in the lungs of HIV-patients and yet no overt pathology has been observed (Mann et al 1997) except in patients with well-preserved CD4 counts, who can presumably mount a cytokine driven T-cell-mediated immune response in the lung (Squire et al 1992;Barry et al 2000).…”

Section: Discussionmentioning

confidence: 99%

Modelling cytomegalovirus replication patterns in the human host: factors important for pathogenesis

et al. 2006

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Human cytomegalovirus can cause a diverse range of diseases in different immunocompromised hosts. The pathogenic mechanisms underlying these diseases have not been fully elucidated, though the maximal viral load during infection is strongly correlated with the disease. However, concentrating on single viral load measures during infection ignores valuable information contained during the entire replication history up to the onset of disease. We use a statistical model that allows all viral load data sampled during infection to be analysed, and have applied it to four immunocompromised groups exhibiting five distinct cytomegalovirus-related diseases. The results show that for all diseases, peaks in viral load contribute less to disease progression than phases of low virus load with equal amount of viral turnover. The model accurately predicted the time of disease onset for fever, gastrointestinal disease and pneumonitis but not for hepatitis and retinitis, implying that other factors may be involved in the pathology of these diseases.

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“…These two patients required mechanical ventilation and were contrasted with nine other HIV infected individuals who all had CD4 counts below 100/l and who developed only a mild respiratory illness with CMV being the only isolate on BAL. 45 The implication of these two severe cases of CMV-P was that their immune responses might have been better preserved, thus contributing to immunopathology. Unfortunately, however, no comment was made on the BAL cell findings in these particular cases.…”

Section: Cytomegalovirus Pneumonitis In Hiv Infectionmentioning

confidence: 99%

Cytopathology or immunopathology? The puzzle of cytomegalovirus pneumonitis revisited

Barry

Jánossy

2000

Bone Marrow Transplant

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Summary:Various hypotheses have been proposed to explain why cytomegalovirus pneumonitis (CMV-P) is frequent and severe in bone marrow transplant patients while remaining rare and mild in HIV infected patients. One hypothesis suggests that CMV-P is an immunopathological condition that is common in bone marrow transplantation (BMT) under the effects of an abnormally regenerating immune system that reacts against CMV infected lung tissue. Such a hypothesis implicates CD4 T lymphocytes as one of the critical cell populations involved in immunopathology and also suggests that this process would be aborted by CD4 T cell deficiency in HIV infection. However, studies correlating the onset of CMV-P with lymphocyte reconstitution following BMT have revealed that CD4 cells are present at very low frequencies in the blood during the early period after transplantation when most cases of CMV-P occur. Furthermore, studies directly investigating bronchoalveolar lavage cell types during episodes of CMV-P in BMT patients have also failed to demonstrate significant CD4 involvement and, instead, have emphasized a predominance of natural killer (NK) cells and CD8 cells. These findings serve as the basis for questioning the validity of a CD4-driven immunopathological model of CMV-P in BMT. On the other hand, a variety of experimental and clinical observations support the protective role of CMV-specific CD3 + CD8 T lymphocytes against CMV in both immunocompetent individuals and BMT patients. In a murine BMT model, adoptive transfer of syngeneic BM cells was associated with massive increases in lung CD8 cells which resulted in the resolution rather than the exacerbation of existing CMV-P. In the light of these findings a more plausible hypothesis for CMV-P in BMT is that during the early period after transplantation adequate protective CD8 responses are absent and an uncontrolled CMV proliferation is allowed to develop. Once a critical viral load is reached a cytokine 'storm' may be triggered in the lung tissue that aggravates direct CMV-associated cytopathic

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Severe cytomegalovirus pneumonitis in HIV infected patients with higher than average CD4 counts.

Cited by 32 publications

References 16 publications

Investigation of CMV disease in immunocompromised patients

Investigation of CMV disease in immunocompromised patients

Modelling cytomegalovirus replication patterns in the human host: factors important for pathogenesis

Cytopathology or immunopathology? The puzzle of cytomegalovirus pneumonitis revisited

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