Cytomegalovirus in the Nervous System of Patients With the Acquired Immune Deficiency Syndrome

Vinters, Harry V.; Kwok, Michael K.; Ho, Hector W.; Anders, Karl H.; Tomiyasu, Uwamie; Wolfson, William L.; Robert, Françoise

doi:10.1093/brain/112.1.245

Cited by 160 publications

(45 citation statements)

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“…CMV frequently disseminates to the CNS in late stages of HIV infection when the CD4 ϩ -T-cell count is low (19,20). CMV is also purported to be a cofactor in AIDS dementia syndrome and can infect the same cells as HIV (5,34,39,49). Clinical manifestations of neurotropic CMV infection of mature CNS may include retinitis, encephalitis, myeloradiculitis, subcortical dementia, obtundation, and other significant neurological deficits, with potentially fatal outcomes (1,3,14,21,33,34,39,49,51).…”

mentioning

confidence: 99%

Systemic Immune Deficiency Necessary for Cytomegalovirus Invasion of the Mature Brain

Reuter¹,

Gomez²,

Wilson³

et al. 2004

J Virol

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mentioning

confidence: 99%

Systemic Immune Deficiency Necessary for Cytomegalovirus Invasion of the Mature Brain

Reuter¹,

Gomez²,

Wilson³

et al. 2004

J Virol

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“…Although CMV infections of the brain in immunocompromised individuals are common, a number of immunocompromised humans show no sign of CMV in the brain for many years (2,21,22,29,30). The study here suggests that one factor that may increase the probability of CMV infection in the immunocompromised brain is the occurrence of some form of brain injury, possibly only a minor injury.…”

Section: Discussionmentioning

confidence: 63%

“…In contrast to the normal mature brain, where CMV infections are uncommon (15, 16), in individuals compromised by human immunodeficiency virus (2,22,30) or during medical immunosuppression associated with organ transplants (10, 21), CMV infections are common. CMV acts as an opportunistic virus that is associated with substantial complications once it has entered the central nervous system (CNS) (1,10,11,15,30,32,33,34). A number of mechanisms keep viruses such as CMV out of the brain; however, once inside the brain, viruses can spread rapidly, particularly within the ventricular systems.…”

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confidence: 99%

Brain Trauma Enhances Transient Cytomegalovirus Invasion of the Brain Only in Mice That Are Immunodeficient

Pol

2009

J Virol

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Cytomegalovirus (CMV) is one of the most common viral pathogens leading to neurological dysfunction in individuals with depressed immune systems. How CMV enters the brain remains an open question. The hypothesis that brain injury may enhance the entrance of CMV into the brain was tested. Insertion of a sterile needle into the brain caused a dramatic increase in mouse CMV in the brains of immunodeficient SCID mice inoculated peripherally within an hour of injury and examined 1 week later; peripheral inoculation 48 h after injury and a 1-week survival resulted in only a modest infection at the site of injury. In contrast, uninjured SCID mice, as well as injured immunocompetent control mice, showed little sign of viral infection at the same time intervals. Direct inoculation of the brain resulted in widespread dispersal and enhanced replication of mCMV in SCID brains tested 1 week later but not in parallel control brains. Differential viremia was unlikely to account for the greater viral load in the SCID brain, since increased mCMV in the blood of SCID compared to controls was not detected until a longer interval. These data suggest that brain injury enhances CMV invasion of the brain, but only when the adaptive immune system is compromised, and that the brain's ability to resist viral infection recovers rapidly after injury.Cytomegalovirus (CMV) is a common virus found in the majority of adult humans. In contrast to the normal mature brain, where CMV infections are uncommon (15, 16), in individuals compromised by human immunodeficiency virus (2,22,30) or during medical immunosuppression associated with organ transplants (10, 21), CMV infections are common. CMV acts as an opportunistic virus that is associated with substantial complications once it has entered the central nervous system (CNS) (1,10,11,15,30,32,33,34). A number of mechanisms keep viruses such as CMV out of the brain; however, once inside the brain, viruses can spread rapidly, particularly within the ventricular systems. Outside the brain, T-and antibodygenerating B lymphocytes of the adaptive immune system, as well as other cells of the systemic immune system, including natural killer and macrophage/monocytes, fight and reduce CMV infections (1,4,8,23). The factors that influence CMV entrance into the adult brain have not been clearly elucidated. In the fetal human brain, in the absence of a developed bloodbrain barrier (BBB), CMV can enter the brain and cause substantial neurological disease (1,3,9).Mouse and human CMV each have genomes of 235 kb of double-stranded DNA, have similar tissue affinity, similar viral morphology and biology, similar ability to achieve long-term latency, and colinear gene sequences with different nucleotide sequences within many genes (15,16,25), suggesting that mouse CMV (mCMV) in many respects parallels its human counterpart.A number of papers studying CMV dispersal in normal and immunocompromised mice reported CMV infection in a number of peripheral organs but did not report CMV in the brain (16,20,23). When a CMV wit...

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“…In general, brain infection by CMV is more common than spinal infection, and the latter is usually manifested by spinal nerve root involvement (i.e., polyradicu litis) [1]. We report the MR imaging findings in an immunosuppressed patient without AIDS in whom clinical and imaging findings were located predominantly in the spinal cord rather than in the brain or spinal nerve roots.…”

mentioning

confidence: 92%

Cytomegalovirus encephalomyelitis: MR imaging findings documenting response to ganciclovir therapy.

Arata¹,

Provenzale²,

Vredenburgh³

1998

American Journal of Roentgenology

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A CNS infection due to cytomega lovirus (CMV) is typically seenin individualswith AIDS and is un common in individuals who are immunosup pressed for other reasons. In general, brain infection by CMV is more common than spinal infection, and the latter is usually manifested by spinal nerve root involvement (i.e., polyradicu litis) [1]. We report the MR imaging findings in an immunosuppressed patient without AIDS in whom clinical and imaging findings were located predominantly in the spinal cord rather than in the brain or spinal nerve roots.The imaging findings of CMV encephalo myelitis are important to recognize because early specific therapy may be life-saving. Case ReportA left breastmasswasfoundat mammogra phy in a 51-year-old woman and was diag nosed as carcinoma by needle biopsy. She underwent left mastectomy and axillary node dissection, which showed multiple lymph nodes positive for the presence of carcinoma. She was treated with a regimen of cyclophos phamide,methotrexate,and 5-fluorouracil. Six years later she developed a left chest wall mass. Fine-needle biopsy showed metastatic breast carcinoma, and she was treated with doxorubicin for 3 months, with a marked de crease in the size of the mass, followed by treatment with cisplatin, carmustine, and cy clophosphamide with stem-cell rescue. Two weeks after completion of chemotherapy, she began to experience leg paresthesias that were initially thought to represent effects of chemo therapy. The paresthesias slowly progressed over the next 6 weeks, consistent with cisplatin sensory polyneuropathy. However, over the course of 1 week, rapidly progressive leg anes thesia, paraparesis,and urinary incontinence developed.Lumbar punctureand MR imaging findings of the brain and total spine 2 days af ter rapid onset of clinical deterioration were negative. The patient was then transferred to our institution for further examination.A secondMR imaging study on hospital day I (7 days after the initial MR imaging study) revealed multiple sites of hyperintense signal on T2-weighted images involving the cervical spinal cord and medulla (Fig. lÃ€).On unenhanced TI-weighted images, the lesions appeared hypointense. After contrast adminis tration, the cervical spine lesions showed ring like enhancement,whereas those within the medulla showed nodular enhancement (Fig. lB). MR imaging of the brain did not reveal other lesions. Because of the possibility that the lesionsrepresentedintramedullary metastases, 18F-fluorodeoxyglucose positron emission to mography was performed on hospital day 8. No increasedmetabolic activity was seenwithin the lesions, and this finding was inter preted as evidence against metastasis. On the assumptionthat the myelopathy could be due to an inflammatoiy demyelinating process, corticosteroid therapy was started on hospital day 3. Follow-up MR imaging on hospital day 9 showed an increase in the size and contrast enhancement of the lesion. A sample of CSF from a secondlumbar punctureon hospital day 13 had positive findings for CMV as deter mined by p...

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Cytomegalovirus in the Nervous System of Patients With the Acquired Immune Deficiency Syndrome

Cited by 160 publications

References 0 publications

Systemic Immune Deficiency Necessary for Cytomegalovirus Invasion of the Mature Brain

Systemic Immune Deficiency Necessary for Cytomegalovirus Invasion of the Mature Brain

Brain Trauma Enhances Transient Cytomegalovirus Invasion of the Brain Only in Mice That Are Immunodeficient

Cytomegalovirus encephalomyelitis: MR imaging findings documenting response to ganciclovir therapy.

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