Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the Lewis rat immunisation with the myelin P0 glycoprotein can induce an inflammatory demyelinating disease of the peripheral nervous system, experimental allergic neuritis (EAN), which has many clinical and histopathological parallels with the human disease the Guillain-Barre syndrome. In view of the reported association of GBS with a number of infectious agents we have investigated whether "molecular mimicry" may occur between microbial antigens and the P0 protein that could possibly trigger a similar pathogenic autoimmune response in man. A computer search of the available protein sequence data bases identified several absolute sequence homologies between P0 and viral proteins that involve five or more consecutive amino acid residues. Four of these sequence homologies involved viral pathogens previously associated with the Guillain-Barre syndrome, namely Epstein-Barr virus (EBV), cytomegalovirus (CMV), Varicella zoster virus (VZV) and human immunodeficiency virus I (HIV I). Although, sequence homologies were also found between viral peptides and the neuritogenic determinants of P0, residues 56-71 and 180-199, these homologies proved incapable of eliciting EAN in the Lewis rat. These observations are discussed with reference to the role that molecular mimicry between T cell epitopes on pathogen derived antigens and the P0 protein may play in the pathogenesis of the Guillain-Barre syndrome.
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PMID:Molecular mimicry and the autoimmune response to the peripheral nerve myelin P0 glycoprotein. 138 42

Four patients with human immunodeficiency virus (HIV) infection who received chronic oral acyclovir therapy for suppression of recurrent varicella zoster or herpes simplex virus infection developed persistent disseminated hyperkeratotic papules that failed to heal with intravenous or high-dose oral acyclovir therapy. Varicella zoster virus, resistant to acyclovir in vitro, was isolated from skin lesions of all four patients. Three patients were adults in whom the acquired immunodeficiency syndrome (AIDS) had been diagnosed 12 to 20 months before isolation of acyclovir-resistant varicella zoster virus. The fourth patient was a perinatally HIV-infected child who developed primary varicella infection at age 7 years when profoundly immunosuppressed (absolute CD4+ lymphocyte count less than 50 cells/microL). Mean antiviral susceptibilities (ED50 values) of the four clinical isolates compared with the ED50 values of the reference strain Oka were 85 compared with 3.3 mumol/L for acyclovir, 1.4 compared with 0.8 mumol/L for vidarabine, and 123 compared with 117 mumol/L for foscarnet. When assayed by [125I]-dC plaque autoradiography, 90% to 100% of the viral isolate populations had altered or no measurable thymidine kinase function. Acyclovir-resistant varicella zoster virus infection may complicate long-term oral acyclovir administration in patients with AIDS and may be associated with the appearance of atypical hyperkeratotic papules.
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PMID:Acyclovir-resistant varicella zoster virus infection after chronic oral acyclovir therapy in patients with the acquired immunodeficiency syndrome (AIDS). 229 95

We report four cases of varicella-zoster pancreatitis in immunocompromised hosts. All 4 patients presented a severe immunodeficiency because of chronic lymphoproliferative disorders (mainly lymphoma and Hodgkin disease) and long-term immunosuppressive therapy. Varicella zoster pancreatitis is a very unusual presentation of varicella-zoster infection. Few cases of pancreatitis occurring after bone marrow transplantation have been reported. All 4 patients presented with acute epigastric pain associated with transient elevation of serum amylase. The vesicular rash followed the presenting symptoms of severe abdominal pain by 8 days. This clinical presentation, occurring in immunocompromised patients, defines a set of symptoms which should lead the physician to suspect varicella-zoster pancreatitis, even in the initial absence of the characteristic skin vesicular eruption. Early institution of antiviral therapy seems mandatory.
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PMID:[Varicella-zoster virus pancreatitis in hematologic diseases]. 852 11

Cases of herpes zoster ophtalmicus (HZO) with delayed contralateral hemiparesis caused by hemispheric stroke secondary to granulomatous angiitis have been reported and are a well-recognized complication of herpes zoster. Similar cases have been reported more recently during infection with human immunodeficiency virus (HIV). We describe two HIV+ patients without any clinical history of zoster dermatitis who developed a sudden hemiparesis followed 2 weeks later for one by an acute retinal necrosis. Computerized tomography (CT) scan, magnetic resonance imaging (MRI), magnetic resonance angiography (MRA), and digital subtraction angiography (DSA) were performed and showed a hemispheric stroke with evidence of a segmental arteritis of the carotid syphon. Varicella zoster virus (VZV) was found in the cerebro spinal fluid (CSF) in the two patients and after puncture of the vitreous fluid of the patient with the acute retinal necrosis. These two cases exemplify the difficulty of diagnosis of stroke in HIV+ patients, which seems to be more frequent than in similarly aged non-infected patients and demonstrates that VZV needs to be taken in consideration and identified even without any past history of zoster dermatitis.
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PMID:Cerebral infarction associated with vasculitis due to varicella zoster virus in patients infected with the human immunodeficiency virus. 986 4

A female patient who developed massive bilateral pneumonia with severe respiratory insufficiency during recovery from varicella, is presented. Blood serologic analyses detected the cause of infection--Mycoplasma pneumoniae, while Streptococcus pneumoniae was isolated by bacteriological examination of the sputum. M. pneumoniae is a causative agent of acute upper and lower respiratory airway infections with a frequently mild clinical picture. This agent rarely provokes massive pneumonia with severe clinical appearance as described in the patient, who had immunodeficiency due to previous infection with Varicella zoster virus.
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PMID:[Massive pneumonia with severe acute respiratory insufficiency after chicken pox in a female patient]. 1093 17

Varicella zoster virus (VZV) infections in human immunodeficiency virus (HIV)-infected patients are known to have a different disease spectrum from that seen in other types of patients. Varicella in children with HIV infection is likely to be more serious than in otherwise healthy children and routine antiviral therapy is recommended. There is evidence that the development of varicella in HIV-infected children is not associated with progression to AIDS, suggesting that it may be safe to immunize HIV-infected children with live attenuated varicella vaccine. There are no published data on varicella in HIV-infected adults, however, probably because most adults have already experienced varicella prior to HIV infection. Zoster in HIV-infected children differs somewhat from that in HIV-infected adults. In particular, HIV-infected children who develop varicella in the setting of severe immunodeficiency are at an especially high risk to develop zoster. Given the low rate of toxicity of aciclovir as well as its ease of administration and its efficacy in hastening the healing of VZV infections, prompt treatment with this antiviral agent is recommended for both HIV-infected children and adults. Foscarnet should be used for zoster that is strongly suspected or proven to be caused by aciclovir-resistant VZV. Patients with HIV for whom there is no evidence of significant immunosuppression and who have not had varicella should be immunized with live attenuated varicella vaccine as a preventative measure for both varicella and zoster. It is hoped that immunization of VZV seropositive HIV-infected patients will decrease the incidence of zoster. Studies to determine this are under way.
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PMID:Prevention and treatment of VZV infections in patients with HIV. 1186 15

Varicella zoster virus (VZV) is a neurotropic human herpesvirus that infects nearly all humans and causes chickenpox (varicella). After chickenpox, VZV becomes latent in cranial nerve, dorsal root, and autonomic nervous system ganglia along the entire neuraxis. Virus reactivation produces shingles (zoster), characterized by pain and rash usually restricted to 1-3 dermatomes. Zoster is often complicated by postherpetic neuralgia (PHN), pain that persists for months to years after rash resolves. Virus may also spread to the spinal cord and blood vessels of the brain, producing a unifocal or multifocal vasculopathy, particularly in immunocompromised individuals. The increased incidence of zoster in elderly and immunocompromised individuals appears to be due to a VZV-specific host immunodeficiency. PHN may reflect a chronic VZV ganglionitis, and VZV vasculopathy is due to productive virus infection in cerebral arteries. Strategies that might boost host cell-mediated immunity to VZV are discussed, as well as the physical state of viral nucleic acid during latency and the possible mechanisms by which herpesvirus latency is maintained and virus is reactivated. A current summary of varicella latency and pathogenesis produced by simian varicella virus (SVV), the counterpart of human VZV, points to the usefulness of a primate model of natural infection to study varicella latency, as well as the experimental model of intratracheal inoculation to study the effectiveness of antiviral agents in driving persistent varicella virus into a latent state.
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PMID:Clinical and molecular pathogenesis of varicella virus infection. 1458 42

Varicella zoster virus (VZV), a ubiquitous neurotropic human herpesvirus, causes chickenpox (varicella) and then remains latent for decades in cranial nerve, dorsal root and autonomic nervous system ganglia along the entire neuraxis. Virus reactivation, most often after age 60, produces shingles (zoster), characterized by pain and rash usually restricted to 1-3 dermatomes. In elderly individuals, zoster is frequently complicated by postherpetic neuralgia (PHN), pain that persists for months to years after the resolution of rash. Virus may also spread beyond ganglia to the spinal cord to cause myelitis, as well as to blood vessels of the brain, producing a unifocal or multifocal vasculopathy. The increased incidence of zoster in the elderly and immunocompromised individuals appears to be due to a VZV-specific host immunodeficiency. Recent studies indicate that PHN may be due to a chronic active VZV ganglionitis, and that VZV vasculopathy is caused by a productive virus infection in cerebral arteries. Since neurological disease produced by VZV is due to reactivation from ganglia, the physical state of viral nucleic acid and expression during latency as well as the possible mechanisms by which VZV latency is maintained and reactivates are discussed. Finally, VZV is an exclusively human herpesvirus, and experimental infection of animals with VZV does not produce disease nor does VZV reactivate from ganglia. Two varicella models in primates have proven useful: one that mimics varicella latency in humans, and one that can be used to study the efficacy of antiviral agent in driving varicella virus back to a latent state.
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PMID:Varicella zoster virus latency, neurological disease and experimental models: an update. 1476 5

The treatment of viral diseases remains one of the major challenges to modern medicine. During the past two decades there has been increased recognition of the consequences of serious viral illnesses that are not controlled by vaccination. These illnesses include human immunodeficiency virus, human herpes viruses, and viruses that cause hepatitis. There are now eight pathogens recognized in the herpes virus family that cause infections in humans. Infections by the herpes viruses are opportunistic and often life-threatening, leading to significant morbidity and mortality in the increasing number of chronically immune compromised individuals such as AIDS patients, cancer patients and transplant recipients on immunosuppressive therapy. Nearly all individuals with AIDS are infected with one or more of the herpes viruses. Antiviral therapy with guanosine nucleoside analogs acyclovir and ganciclovir has had a major impact on diseases caused by herpes simplex virus type-1 and type-2 (HSV-1, HSV-2), Varicella zoster virus (VZV), and human cytomegalovirus (HCMV) but development of resistant virus strains and the absence of any effective treatment for other members of the herpes family provide a stimulus for increased search of new agents effective against various herpes viruses. Pyrimidine nucleosides have taken up an important role in the therapy of virus infection. Significant progress in the study of anti-herpes nucleosides has been made by the advent of 5-substituted pyrimidine nucleosides such as 5-iodo-, 5-ethyl-, 5-(2-chloroethyl)-, and (E)-5-(2-bromovinyl)- derivatives of 2'-deoxyuridine. These are highly specific inhibitors of HSV-1, HSV-2, and/or VZV infections. However, Epstein Barr virus (EBV) and HCMV are much less sensitive to these agents. In 5-substituted pyrimidine nucleosides the nature of substituents, particularly at the C-5 position, has been found to be an important determinant of anti-herpes activity. Structural requirements at the C-2 carbon of the 5-substituent of pyrimidine nucleosides have been well established for anti-herpes activity. However, there is little qualitative or mechanistic knowledge of the derivatives with substitution at the C-1 carbon of the 5-substituent of pyrimidine nucleosides. During the last few years of our research, we have investigated a variety of C-1 functionalized substituents at the 5-position of the pyrimidine nucleosides to determine their usefulness as antiviral (herpes) agents. In the 5-(1-substituted) group of pyrimidine nucleosides, we demonstrated that novel substituents present at the C-1 carbon of the 5-side chain of the pyrimidine nucleosides are important determinants of potent and broad spectrum antiviral (herpes) activity including EBV and HCMV. In this article the work on design, synthesis and structure activity relationships of several 5-[(1-substituted) alkyl (or vinyl)] pyrimidine nucleoside derivatives as potential inhibitors of herpes viruses is reviewed.
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PMID:5-(1-Substituted) alkyl pyrimidine nucleosides as antiviral (herpes) agents. 1554 74

Herpes zoster is an infection caused by reactivation of the latent varicella virus in the sensory ganglia. The mechanisms responsible for Varicella zoster virus (VZV) reactivation are poorly understood. Yet, it is believed that decreased cellular immunity can be a trigger for it's reactivation. The occurrence of herpes zoster in young people may point to an underlying immunodeficiency. Therefore, the possibility of concomitant HIV infection must be eliminated. Herpes zoster manifests as a vesicular rash along a sensory dermatome, usually preceded by pain or paresthesia of the involved cutaneous area. The most commonly affected dermatomes are those of the thorax and abdomen, followed by the cranial nerves, especially the trigeminal nerve. The maxillary nerve is the least frequently affected branch of the trigeminal nerve and only rarely causes ocular injury. This is a case history of a young patient infected with VZV involving the maxillary branch of the trigeminal nerve, complicated by secondary bacterial infection of the ipsilateral hemiface. The literature regarding the epidemiology, pathogenesis, complications and the proper treatment of herpes zoster is reviewed with an emphasis on the involvement of cranial nerves.
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PMID:[Varicella zoster virus infection involving the maxillary branch of the trigeminal nerve]. 1735 73


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