Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001486 (Adenovirus)
 3,125 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of febrile ulceronecrotic Mucha-Habermann's is presented. This disorder is a severe form of pityriasis lichenoides et varioliformis acuta (PLEVA) characterized by the sudden eruption of diffuse coalescent ulcerations associated with high fever. In the present case the disease was preceded by the milder typical form of PLEVA. Histologically a leukocytoclastic vasculitis was seen in addition to the usual lymphocytic perivascular and lichenoid infiltrate. During the course of the disease the patient developed an interstitial pneumonitis which resolved concomitantly with the cutaneous lesions. Adenovirus type II recovered at the height of the illness from the patient's urine may have etiologic implications in the pathogenesis of the disease.
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PMID:Febrile ulceronecrotic Mucha-Habermann's disease with interstitial pneumonitis. 43 96

Non-specific interstitial pneumonia (NIP) occurs frequently in patients with HIV-infection. To elucidate the etiology of this pulmonary disorder, we searched for 13 different microorganisms in transbronchial biopsies from 15 patients with NIP, 15 patients with Pneumocystis carinii pneumonia (PCP) and 20 patients with lung diseases not related to HIV-infection using monoclonal antibodies and the APAAP- or PAP-technique for immunostaining. Chlamydia trachomatis and parainfluenza III were detected frequently and in great number. Adenovirus, influenza B, varicella zoster and cytomegalovirus were also found frequently, but not in great number. Measles virus, respiratory syncytial virus, influenza A and herpesviruses 1&2 were not found. Also not found were parainfluenza I, mycoplasma pneumoniae and coronavirus. In seven out of fifteen NIP patients at least one organism was shown, compared to nine out of fifteen patients with PCP and eight out of twenty patients in the control group.
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PMID:Non-specific interstitial pneumonia (NIP): immunohistologic screening of etiologic agents. 789 90

We have encountered a 12-year-old girl with acute respiratory disease including pneumonia caused by adenovirus type 7. While being followed-up for bronchial asthma, she developed this disease with dyspnea accompanied by high fever, pharyngalgia and a dry cough subsequent to a slight fever. Adenovirus type 7 was separated and identified from the pharyngeal smear. Additionally, perfusion scintigraphy of the lungs presented evidence of interstitial pneumonia. with these findings and the clinical course put together, this case was diagnosed as having acute respiratory disease with pneumonia caused by adenovirus type 7. Thereafter, perfusion scintigraphy of the lungs continued showing interstitial shadows, which suggested the presence of severe sequlae of the lung. Formerly the separation rate of adenovirus type 7 was low in Japan, but the rate has tended to increase in cities in recent years. Cases presenting such acute, severe respiratory symptoms are expected to increase in the future, and clinically we consider to be our case important enough to be reported.
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PMID:[A 12-year-old girl with acute respiratory disease with pneumonia caused by adenovirus type 7]. 869

We present a comparative histopathological study of both acute and chronic human adenovirus pneumonia, with reference to the cellular and extracellular matrix components. Seventeen lungs from autopsied patients whose ages ranged from 2 to 60 months were studied. Adenovirus types 1, 2, 3, 5, and 7 were isolated from 15 patients with acute lung disease, and types 2 and 7 were isolated from the other two patients with chronic pulmonary illness. The results indicated the occurrence of two basic patterns of adenovirus interstitial pneumonia (1) classic pattern (acute), characterized by necrosis and degeneration and many type II pneumocytes with intranuclear inclusion bodies, which were positive for adenovirus DNA by in situ hybridization, and (2) proliferative or proliferative-productive pattern (chronic), which presented with diffuse pulmonary fibrosis and the interstitial proliferation of fibroblast-like cells, compatible with myofibroblasts (positive for vimentin and alpha smooth muscle actin), and increase in collagen types I and III, elastic fibers, and proteoglycans. Alveolar collapse appears to be an important pathogenetic mechanism in the development of this pattern.
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PMID:Acute and chronic human adenovirus pneumonia: cellular and extracellular matrix components. 902 50

Adenovirus (ADV) is increasingly recognized as a cause of morbidity and mortality in transplant recipients, but ADV pneumonitis has rarely been reported after lung transplantation. The few reported instances of ADV pneumonitis occurred mostly in children immediately after lung transplantation suggesting "primary" infection. We report a fatal case of ADV pneumonitis occurring in an adult, 4 years after unilateral lung transplantation, in whom the premortem diagnosis was not determined. Autopsy revealed severe necrotizing bronchitis, bronchiolitis, and interstitial pneumonitis. Characteristic smudgy intranuclear inclusions, immunohistochemistry for viral protein, in situ hybridization for viral genome, and postmortem lung cultures established ADV as the etiologic agent. ADV can cause fatal, occult respiratory infection in adult lung transplant recipients, remote from transplant surgery.
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PMID:Late fatal adenovirus pneumonitis in a lung transplant recipient. 950 Jun 42

Adenovirus type 5 (Ad5) E3 region proteins abrogate Ad pathogenicity in the lungs of cotton rats. Our use of Ad4-HIV E3-deleted (DeltaE3) recombinants as vaccines necessitates further examination of these viruses for enhanced pathogenesis. Equivalent infectious doses of Ad4 wild-type (Ad4WT), Ad4DeltaE3, and two recombinants: Ad4DeltaE3HIVenv and Ad4DeltaE3HIVgag, were inoculated intranasally into cotton rats. Ad4 viruses did not replicate in the lungs, but caused mild pathologic effects, including peribronchiolitis, bronchitis, alveolitis, and interstitial pneumonia. As found previously for Ad5, deletion of Ad4 E3 genes resulted in increased lung pathology. Surprisingly, insertion of HIV genes into this region significantly restored protection attributed to E3 gene products, diminishing overall pathologic effects to Ad4WT levels (P < 0.0001). Similarly, following administration of equivalent particle numbers of the four viruses, only Ad4DeltaE3 caused increased overall pathology, while the two HIV recombinant viruses showed effects comparable to Ad4WT (P < 0.01). Our observation that Ad4DeltaE3HIV recombinants are as safe in cotton rats as Ad4WT encourages their continued development as AIDS vaccines.
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PMID:Insertion of HIV-1 genes into Ad4DeltaE3 vector abrogates increased pathogenesis in cotton rats due to E3 deletion. 1187 13

In two guinea pigs (five years old, neutered male, and two and a half months old male, respectively) suffering from interstitial pneumonia, multinucleated giant cells were observed histologically in lungs, spleen and liver. The giant cells showed intranuclear, pale basophilic inclusions. Adenovirus could be demonstrated by electron microscopy.The multinucleated cells are supposed to be of histiocytic origin, since they contained variable amounts of haemosiderin in their cytoplasm. Formation of histiocyte-derived syncytia as a result of virus-induced cell fusion is discussed.
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PMID:[Appearance of multinucleated giant cells in association with an adenovirus infection in two guinea pigs]. 1717 35