Serologic Evidence of Human Immunodeficiency Virus Infection of the Central Nervous System in African Patients with Acquired Immunodeficiency Syndrome

Kaiser, Reinhard; Dörries, Rüdiger; Meulen, Jan ter; Kidenya, J. J.; Pöllath, M.; Fleischer, K; Meulen, V. ter

doi:10.1159/000116621

Cited by 10 publications

(2 citation statements)

References 25 publications

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“…Intrathecal secretion against specific HIV proteins has been found with variable frequencies (Goudsmit et al, 1987;Chiodi et al, 1988aChiodi et al, , 1988bGrimaldi et al, 1988;Kaiser et al, 1989;Lolli et al, 1990;Goswami et al, 1991;Fainardi et al, 2001). Intrathecal IgG OCB synthesis against HIV occurs in up to 70% of patients (Bukasa et al, 1988;Chiodi et al, 1988a;McArthur et al, 1989;Singer et al, 1994;Gisslen et al, 1999a;Fainardi et al, 2001) but OCB against HIV antigens are detected by immunoblotting in up to 87% (Bukasa et al, 1988;Dorries et al, 1989;Kaiser et al, 1990). IgG HIV antibody index is elevated (N1.5) in the majority (75-85%) of patients from whom HIV-RNA is recovered from the CSF.…”

Section: Intrathecal Hiv-specific Igg Synthesis Is Frequently Observementioning

confidence: 99%

Compartmentalized intrathecal immunoglobulin synthesis during HIV infection — A model of chronic CNS inflammation?

Bonnan¹,

Barroso²,

Demasles³

et al. 2015

Journal of Neuroimmunology

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HIV infects the central nervous system (CNS) during primary infection and persists in resident macrophages. CNS infection initiates a strong local immune response that fails to control the virus but is responsible for by-stander lesions involved in neurocognitive disorders. Although highly active anti-retroviral therapy now offers an almost complete control of CNS viral proliferation, low-grade CNS inflammation persists. This review focuses on HIV-induced intrathecal immunoglobulin (Ig) synthesis. Intrathecal Ig synthesis early occurs in more than three-quarters of patients in response to viral infection of the CNS and persists throughout the course of the disease. Viral antigens are targeted but this specific response accounts for <5% of the whole intrathecal synthesis. Although the nature and mechanisms leading to non-specific synthesis are unknown, this prominent proportion is comparable to that observed in various CNS viral infections. Cerebrospinal fluid-floating antibody-secreting cells account for a minority of the whole synthesis, which mainly takes place in perivascular inflammatory infiltrates of the CNS parenchyma. B-cell traffic and lineage across the blood-brain-barrier have not yet been described. We review common technical pitfalls and update the pending questions in the field. Moreover, since HIV infection is associated with an intrathecal chronic oligoclonal (and mostly non-specific) Ig synthesis and associates with low-grade axonal lesions, this could be an interesting model of the chronic intrathecal synthesis occurring during multiple sclerosis.

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Section: Intrathecal Hiv-specific Igg Synthesis Is Frequently Observementioning

confidence: 99%

Compartmentalized intrathecal immunoglobulin synthesis during HIV infection — A model of chronic CNS inflammation?

Bonnan¹,

Barroso²,

Demasles³

et al. 2015

Journal of Neuroimmunology

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“…Lymphocytes generally require activation prior to entry into the CNS [20] but antigen specificity is not necessary for entry. Further evidence supporting the fact that immunological responses can occur in the CNS is supported by the presence of antibody-secreting plasma cells in the CNS [21, 22] and the therapeutic efficacy of systemically administered antibodies for the treatment of multiple sclerosis [23] and Alzheimer disease [24]. Both peptide vaccination approaches and direct instillation of glioma-specific antibodies intratumorally have been shown to mediate their in vivo efficacy via antibody dependent cellular cytotoxicity (ADCC) [25, 26].…”

Section: Central Nervous System Immunitymentioning

confidence: 99%

The PEPvIII-KLH (CDX-110) vaccine in glioblastoma multiforme patients

Heimberger

Sampson

2009

Expert Opinion on Biological Therapy

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Conventional therapies for glioblastoma multiforme (GBM) fail to target tumor cells exclusively resulting in non-specific toxicity. Immune targeting of tumor-specific mutations may allow for more precise eradication of neoplastic cells. The epidermal growth factor receptor variant III (EGFRvIII) is a tumor-specific mutation that is widely expressed on GBM and other neoplasms and its expression enhances tumorigenicity. This in-frame deletion mutation splits a codon resulting in a novel glycine at the fusion junction producing a tumor-specific epitope target for cellular or humoral immunotherapy. We have previously shown that vaccination with a peptide that spans the EGFRvIII fusion junction (PEPvIII-KLH/CDX-110) is an efficacious immunotherapy in syngeneic murine models. In this review, we summarize our results in GBM patients targeting this mutation in multiple, multi-institutional Phase II immunotherapy trials. These trials demonstrated that a selected population of GBM patients who received the vaccines targeting EGFRvIII had an unexpectedly long survival time. Further therapeutic strategies and potential pitfalls using this approach are discussed.

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Hormonal Influences on the Pelvic Floor

Davila¹

Pelvic Floor Dysfunction

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Reproductive hormones, especially estrogen, have a significant impact on pelvic floor function. Hormonal changes that occur during a woman's lifespan impact many aspects of female physiology. With the onset of menopause, it becomes evident that estrogen sensitivity is greatest in the central nervous system and the genital tissues.The most frequently occurring initial symptoms of estrogen deprivation include hot flushes, mood changes, and emotional irritability. These central nervous system symptoms are promptly reversible with systemic estrogen replacement. More prolonged duration of estrogen deprivation will lead to other known consequences such as osteoporosis and urogenital atrophy. It is estimated that 80% of postmenopausal women have hot flushes, and that not all women will develop osteoporosis. However, urogenital atrophy occurs universally. Interestingly, many women with urogenital atrophy are asymptomatic.1 Many treatments are currently available for prevention of and therapy for loss of bone mineral content. However, local estrogen therapy is the only means of treating symptoms and signs of urogenital atrophy.As related to the pelvic floor, urogenital atrophy is present at both ends of the reproductive cycle, and consequences such as labial fusion may be present both premenarchally as well as postmenopausally. After the onset of menopause, hypoestrogenism is expressed in the lower genitourinary tract by thinning of the vaginal and urethral mucosa, as well as other well-recognized changes (Table 11-1.1). Estrogen receptors have been found in most body tissues. The presence of estrogen receptors in the pelvic floor mucosa has been demonstrated, as has the importance of the estrogen-replete state in physiologic cellular proliferation.2,3 The implications of the lack of estrogen on urogenital well-being will be discussed in this chapter. Vaginal AtrophyThe urethral and vaginal mucosas are rich in estrogen receptors and share a common embryologic origin from the urogenital sinus. As such, these tissues are exquisitely sensitive to estrogen deprivation, and symptoms may appear promptly as soon as estrogen levels begin to decline. Vaginal atrophy will present with a variety of symptoms along a continuum of severity. Symptoms are typically vaginal dryness and associated dyspareunia, which may be initially presented as vaginal irritation. This will progress to loss of vaginal rugation and development of a progressively pale, hypovascular mucosa. Eventually, a thin inflammatory exudate can develop, sometimes in large quantities. This may result in a watery vaginal discharge that on microscopic examination is replete with inflammatory and basal squamous epithelial cells, but with no evidence of bacterial infection. As with other more obvious mucosal hypoestrogenic states, a chronic watery vaginal discharge without an infectious cause in a postmenopausal woman warrants a course of local estrogen therapy. Up to this stage of atrophy progression, resultant changes are readily reversible with local estrogen administrat...

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Serologic Evidence of Human Immunodeficiency Virus Infection of the Central Nervous System in African Patients with Acquired Immunodeficiency Syndrome

Cited by 10 publications

References 25 publications

Compartmentalized intrathecal immunoglobulin synthesis during HIV infection — A model of chronic CNS inflammation?

Compartmentalized intrathecal immunoglobulin synthesis during HIV infection — A model of chronic CNS inflammation?

The PEPvIII-KLH (CDX-110) vaccine in glioblastoma multiforme patients

Hormonal Influences on the Pelvic Floor

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