Two cases of necrotizing myelopathy associated with malignancy caused by herpes simplex virus type 2

Iwamasa, Teruo; Utsumi, Yasufumi; Sakuda, Hitoshi; Yoshitake, Hidenori; Kakazu, Tomokazu; Nakagawa, Masanori

doi:10.1007/bf00687754

Cited by 32 publications

(17 citation statements)

References 10 publications

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“…In previous reports, HSV myelitis was accompanied by conditions that reduce immunologic competence, such as acquired immunodeficiency syndrome [5,6], malignancies [7,8], and diabetes mellitus [3]. Ellie et al [12] and Flope et al [13] have recently reported HSV myelitis in nonimmunocompromised patients.…”

Section: Discussionmentioning

confidence: 99%

Herpes simplex Virus Myelitis: Clinical Manifestations and Diagnosis by the Polymerase Chain Reaction Method

Nakajima¹,

Furutama²,

Kimura³

et al. 1998

Eur Neurol

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Herpes simplex virus (HSV) myelitis has previously been reported to be a form of acute ascending necrotizing myelitis caused by HSV type 2 (HSV-2). We studied neurological symptoms, clinical course, magnetic resonance imaging (MRI) findings, and diagnosis by polymerase chain reaction (PCR) methods in 9 patients with HSV myelitis. In 6 cases, disease onset was marked by sensorimotor disturbances of lower extremities and urinary disturbances, with the transverse myelopathy gradually ascending to the cervicothoracic spinal cord level. The other 3 cases showed transverse myelopathy without an ascending pattern. Six cases showed acute progression, while 3 cases showed a subacute course. There were 2 cases with recurrent episodes. Three patients recovered, however, in the remaining 6 patients severe sequelae such as paraplegia persisted despite antiviral therapy. MRI showed a hyperintense lesion on T2-weighted images. Gadolinium enhancement was observed in 2 cases, and 1 case showed a hyperintense lesion both on T1- and on T2-weighted images, suggesting hemorrhagic necrosis. HSV-2 was detected by PCR techniques in all 6 cases with an ascending pattern. HSV-1 DNA was detected in 2 and HSV-2 DNA in 1 of the 3 cases with a nonascending pattern. Our findings demonstrate diverse clinical manifestations of HSV myelitis.

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Section: Discussionmentioning

confidence: 99%

Herpes simplex Virus Myelitis: Clinical Manifestations and Diagnosis by the Polymerase Chain Reaction Method

Nakajima¹,

Furutama²,

Kimura³

et al. 1998

Eur Neurol

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“…22,23 Indeed, previous reports have shown that some ATL patients are infected with these 2 pathogens. 24,25 Using these 2 infection models, we demonstrated that sHBZ suppresses cell-mediated immunity. Furthermore, we determined the molecular mechanism of this HBZ-mediated immune suppression.…”

Section: Introductionmentioning

confidence: 94%

HTLV-1 bZIP factor impairs cell-mediated immunity by suppressing production of Th1 cytokines

Sugata

Satou

Yasunaga

et al. 2012

Blood

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IntroductionHuman T-cell leukemia virus type 1 (HTLV-1) is a retrovirus that mainly infects CD4 T cells, 1 a critical cell population for the host defense against foreign pathogens. HTLV-1 is known as the causal agent of adult T-cell leukemia (ATL), 2-4 a leukemia derived from CD4 T cells, and chronic inflammatory diseases, including HTLV-1-associated myelopathy/tropical spastic paraparesis, 5,6 alveolitis, 7 and uveitis. It has also been recognized that HTLV-1 infection is complicated by opportunistic infections caused by Pneumocystis jiroveci, herpes zoster virus, cytomegalovirus, or Strongyloides stercoralis. 8 However, the mechanism by which HTLV-1 causes immune deficiency has remained unknown.Another human pathogenic retrovirus, HIV, replicates vigorously in vivo and produces a large number of virions. As a result of abundant viral production, HIV-infected CD4 T cells proceed to apoptosis, a phenomenon that eventually results in AIDS. In contrast, HTLV-1 increases its copy number primarily in the form of a provirus, by promoting the clonal proliferation of infected host CD4 T cells. 9,10 Despite this opposite effect on CD4 T-cell homeostasis compared with HIV, HTLV-1 infection and ATL are frequently accompanied by a deficiency of cellular immunity resembling that seen with AIDS.HTLV-1 encodes several regulatory and accessory genes in the viral genome. 1,11 The viral proteins expressed by the integrated provirus control viral gene transcription and induce host cell proliferation, enabling HTLV-1 to achieve persistent infection. Among the viral genes of HTLV-1, HTLV-1 bZIP factor (HBZ), which is encoded in the minus strand, 12 is a constitutively expressed viral gene. 13 It has been reported that there are 2 major transcripts of the HBZ gene: spliced HBZ (sHBZ) and unspliced HBZ (usHBZ). 14 Based on the findings that sHBZ is more abundantly expressed than usHBZ 15 and that sHBZ has a functionally stronger effect than usHBZ, 16 we focused on sHBZ in this study.Recently, we have reported that sHBZ expression increases the number of regulatory T cells (Tregs) by inducing transcription of the Foxp3 gene in transgenic mice that express the HBZ gene in CD4 T cells (HBZ-Tg mice). 17 An increase in Tregs might be implicated in the immunodeficiency observed in ATL patients. Furthermore, previous studies have reported that HBZ suppresses host cell-signaling pathways that are critical for T-cell receptor signaling in the immune response, such as the NF-B 18 and AP-1 pathways. 19 These findings led us to hypothesize that HBZ might have important roles in the dysregulation of cellular immunity associated with HTLV-1 infection.To verify this hypothesis, we used HBZ-Tg mice that express sHBZ in CD4 T cells and studied well-established infection models of 2 pathogens. The first model involves intravaginal viral infection with herpes simplex virus type-2 (HSV-2). IFN-␥ production by CD4 T cells is critical for the exclusion of HSV-2 from the host. 20,21 The other model involves infection with the Gram-positive intracellular b...

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“…Neuropathological findings in herpes virus associated necrotizing myeloradiculitis include extensive necrotic and hemorrhagic changes associated with necrotizing vasculitis and perivascular lymphocytic infiltration involving both gray and white matter as well as spinal roots 10,14 .…”

Section: Discussionmentioning

confidence: 99%

CMV and HSV-2 myeloradiculitis in an HIV infected patient

Pinto

Santos

Correa

et al. 2011

Rev. Inst. Med. trop. S. Paulo

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SUMMARYWhile CMV myeloradiculitis is a known complication in AIDS patients with severe immunosuppression, HSV-2 necrotizing myeloradiculitis is rare and often associated with disabling a fatal outcome. We hereby describe a 46 year-old HIV infected patient with profound and sustained immunosuppression who presented with an acute ascending paraparesis and urinary retention. Lumbar spine MRI showed contrast enhancement at the conus medullaris and cauda equine, and both CMV and HSV-2 CSF PCR were positive. Despite treatment, the patient died 20 days later. We review the main diagnostic and therapeutic aspects of herpes virus associated myeloradiculitis and discuss the approach in similar cases.

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Two cases of necrotizing myelopathy associated with malignancy caused by herpes simplex virus type 2

Cited by 32 publications

References 10 publications

Herpes simplex Virus Myelitis: Clinical Manifestations and Diagnosis by the Polymerase Chain Reaction Method

Herpes simplex Virus Myelitis: Clinical Manifestations and Diagnosis by the Polymerase Chain Reaction Method

HTLV-1 bZIP factor impairs cell-mediated immunity by suppressing production of Th1 cytokines

CMV and HSV-2 myeloradiculitis in an HIV infected patient

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