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)

The human immunodeficiency virus type-1 (HIV-1)-encoded vif protein is essential for viral replication, virion production, and pathogenicity. HIV-1 Vif interacts with the endogenous human APOBEC3G protein (an mRNA editor) in target cells to prevent its encapsidation into virions. Some studies have established targets within the HIV-1 vif gene that are important for its biologic function; however, it is important to determine effective therapeutic targets in vif because of its critical role in HIV-1 infectivity and pathogenicity. The present study demonstrates that virions generated in transfected HeLa-CD4+ cells, especially from HIV-1 vif frame-shift mutant (3' delta vif; 5561-5849), were affected in splicing and had low infectivity in MT-4 cells. In addition, HIV-1 vif antisense RNA fragments constructed within the same region, notably the region spanning nucleic acid positions 5561-5705 (M-3'-AS), which corresponds to amino acid residues 96-144, significantly inhibited HIV-1 replication in MT-4 and reduced the HIV-1 vif mRNA transcripts and reporter gene (EGFP) expression. The generated virions showed low secondary infection in H9 cells. These data therefore suggest that the middle to the 3' end of vif is important for its biological activity in the target cells.
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PMID:The middle to 3' end of the HIV-1 vif gene sequence is important for vif biological activity and could be used for antisense oligonucleotide targets. 1643 45

Tuberculosis of the stomach is quite rare, both as a primary or secondary infection. It can present as a facet of a multiorgan disease process or may result from immunodeficiency. Here, we report a rare, interesting case of gastric tuberculosis which morphologically mimicked advanced gastric cancer in a young, immunocompetent patient presenting with hematemesis and melena. The disease was diagnosed by biopsy, and responded well to antituberculosis medication without surgery. Clinicians must bear in mind that, even in the absence of immunodeficiency, as in this case, tuberculosis can involve any site in the gastrointestinal tract and may present with a variety of characteristics. Gastric tuberculosis should always be part of the differential diagnosis of chronic infiltrative lesions in the stomach.
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PMID:A case of gastric tuberculosis mimicking advanced gastric cancer. 1664 68

Human immunodeficiency virus (HIV)-1 causes lung disease by increasing the host's susceptibility to pathogens. HIV-1 also causes an increase in systemic oxidative/nitrosative stress, perhaps enhancing the deleterious effects of secondary infections. Here we examined the ability of HIV-1 proteins to increase lung oxidative/nitrosative stress after lipopolysaccharide (LPS) (endotoxin) administration in an HIV-1 transgenic mouse model. Lung oxidative/nitrosative stress biomarkers studied 3 and 6 h after LPS administration were as follows: lung edema, tissue superoxide, NO metabolites, nitrotyrosine, hydrogen peroxide, and bronchoalveolar lavage fluid (BALF) glutathione (GSH). Blood serum cytokine levels were quantified to verify immune function of our nonimmunocompromised animal model. Results indicate that 3 h after LPS administration, HIV-1 transgenic mouse lung tissue has significantly greater edema and superoxide. Furthermore, NO metabolites are significantly elevated in HIV-1 transgenic mouse BALF, lung tissue, and blood plasma compared with those of wild-type mice. HIV-1 transgenic mice also produce significantly greater lung nitrotyrosine and hydrogen peroxide than wild-type mice. In addition, HIV-1 transgenic mice produce significantly less BALF GSH than wild-type mice 3 h after LPS treatment. Without treatment, serum cytokine levels are similar for HIV-1 transgenic and wild-type mice. After treatment, serum cytokine levels are significantly elevated in both HIV-1 transgenic and wild-type mice. Therefore, HIV-1 transgenic mice have significantly greater lung oxidative/nitrosative stress after endotoxin administration than wild-type mice, independent of immune function. These results indicate that HIV-1 proteins may increase pulmonary complications subsequent to a secondary infection by altering the lung redox potential.
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PMID:HIV-1-induced pulmonary oxidative and nitrosative stress: exacerbated response to endotoxin administration in HIV-1 transgenic mouse model. 1672 26

Simian-Human immunodeficiency virus is a chimeric virus which, in rhesus macaques (Macacca mulatta) closely imitates immunodeficiency virus infection in human (HIV). A relatively new way to study pathogenesis of viral infection is to study alterations in host gene expression induced by the virus. SHIV infection with certain strains does not result in clinical signs. We hypothesized that alterations in gene expression relating to the immune system would be present in SHIV-infected animals despite the lack of clinical signs. Splenic tissue from four adult male Indian-origin Rhesus monkeys serologically positive for non-pathogenic SHIV 89.6 was processed by cDNA microarray analysis. Results were compared with the corresponding outcome using splenic tissues from four unexposed adult male Rhesus monkeys. Subsequent gene analysis confirmed statistically significant variations between control and infected samples. Interestingly, SHIV-infected monkeys exhibited altered expression in genes related to apoptosis, signal transduction, T and B lymphocyte activation and importantly, to immune regulation. Although infected animals appeared asymptomatic, our study demonstrated that SHIV-infected monkeys cannot reliably be used in studies of other infectious agents as their baseline gene expression differs from that of normal Rhesus monkeys. The gene expression differences in SHIV-infected animals relative to uninfected animals offer additional clues to the pathogenesis of altered immune function in response to secondary infection.
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PMID:Altered gene expression in asymptomatic SHIV-infected rhesus macaques (Macacca mulatta). 1695 15

Systemic vasculitis is a rare but devastating problem in patients with human immunodeficiency virus (HIV). The coinfection with hepatitis C virus (HCV) further complicates the clinical management. We report a 46-year-old woman coinfected with HCV and HIV with a CD4 count of 950/mm who presented with a life-threatening vasculitis of the lungs, kidneys, and skin and who initially responded after use of corticosteroids and then 2 monthly pulses of i.v. cyclophosphamide. Her condition deteriorated when she was switched to azathioprine. Ultimately, the patient died of neutropenic sepsis. On the basis of our experience and an analysis of the literature, we suggest that monthly pulsed i.v. cyclophosphamide and steroids might be used as an induction therapy, followed by antiviral treatment for patients with HIV, HCV, and a life-threatening ischemic vasculitis if the CD4 count is >400/mm. For patients in this complex condition who are receiving immunosuppressants close surveillance for signs of secondary infection, and prophylactic trimethoprim/sulfamethoxazole, are advised. The use of interferon alpha, ribavirin, i.v. immunoglobulin, and plasmapheresis are alternatives for patients with milder vasculitis.
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PMID:Systemic Necrotizing Vasculitis in a Patient Co-infected with Human Immunodeficiency Virus and Hepatitis C. 1907 77

Both surgical and endovascular grafts have the rare risk of late secondary infection. Treatment varies based on the clinical setting, but in general the recommendations are that infected endografts be removed and reconstruction performed. In the abdominal aorta this may vary from homograft or other impregnated grafts to excision and extra-anatomic bypass. We discuss an unusual case which we believe serves as a useful review of this still debated area. A 58-year-old male presented with abdominal and back pain. Prior history was notable for human immunodeficiency virus positive status, pulmonary embolism (currently on Coumadin) and two years previously repair of a saccular infra-renal aneurysm with tube graft. The week prior to the onset of symptoms he suffered a noticeable scratch from his cat. Blood cultures were positive for pasturella multicoda. He was transferred to our institution and underwent resection and explantation, with homograft reconstruction. At one year he is alive and well.
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PMID:Pasturella multicoda infection of an abdominal aortic endograft. 2349 55

A 1-yr-old albino male corn snake (Elaphae guttata guttata), which was part of a large breeding stock, was presented to the University of Florida, College of Veterinary Medicine, Zoo and Exotic Animal Clinic with a history of anorexia for 2 wk and progressively declining body condition. The animal was euthanized due to a poor prognosis. Histopathology, electron microscopy, and polymerase chain reaction analysis on tissues revealed concurrent infection with adenovirus and Cryptosporidium. Primary infection with adenovirus could have caused immunodeficiency in the snake, thus predisposing it to secondary infection with Cryptosporidium. To the authors' knowledge, this is the first report of co-infection of adenovirus and Cryptosporidium in a Colubrid species of snake.
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PMID:Adenovirus and cryptosporidium co-infection in a corn snake (Elaphae guttata guttata). 2350 34

Buruli ulcer is a chronic and infectious skin disease, caused by Mycobacterium ulcerans. It leads to large skin ulceration and sometimes bone infection which is responsible for deformities. Here, we report a case of multifocal form of Buruli ulcer associated with secondary infection in a 46-year-old human immunodeficiency virus (HIV) positive woman. The antimycobacterial drugs combined to surgery allowed curing this multifocal case and rose up two relevant issues: the susceptibility of immune reconstitution inflammatory syndrome (IRIS) occurrence and Mycobacterium dissemination. The deep immune depression, the underline biological, and clinical disorders of the patient might contribute to IRIS occurrence and Buruli ulcer dissemination. Future investigations have to be conducted on the mechanism of IRIS on set and on Mycobacterium ulcerans dissemination after ARV drugs initiation and the patient related underline clinical or biological disorders.
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PMID:Multifocal Buruli Ulcer Associated with Secondary Infection in HIV Positive Patient. 2445 98

Neck masses in children usually fall into one of three categories: developmental, inflammatory/reactive, or neoplastic. Common congenital developmental masses in the neck include thyroglossal duct cysts, branchial cleft cysts, dermoid cysts, vascular malformations, and hemangiomas. Inflammatory neck masses can be the result of reactive lymphadenopathy, infectious lymphadenitis (viral, staphylococcal, and mycobacterial infections; cat-scratch disease), or Kawasaki disease. Common benign neoplastic lesions include pilomatrixomas, lipomas, fibromas, neurofibromas, and salivary gland tumors. Although rare in children, malignant lesions occurring in the neck include lymphoma, rhabdomyosarcoma, thyroid carcinoma, and metastatic nasopharyngeal carcinoma. Workup for a neck mass may include a complete blood count; purified protein derivative test for tuberculosis; and measurement of titers for Epstein-Barr virus, cat-scratch disease, cytomegalovirus, human immunodeficiency virus, and toxoplasmosis if the history raises suspicion for any of these conditions. Ultrasonography is the preferred imaging study for a developmental or palpable mass. Computed tomography with intravenous contrast media is recommended for evaluating a malignancy or a suspected retropharyngeal or deep neck abscess. Congenital neck masses are excised to prevent potential growth and secondary infection of the lesion. Antibiotic therapy for suspected bacterial lymphadenitis should target Staphylococcus aureus and group A streptococcus. Lack of response to initial antibiotics should prompt consideration of intravenous antibiotic therapy, referral for possible incision and drainage, or further workup. If malignancy is suspected (accompanying type B symptoms; hard, firm, or rubbery consistency; fixed mass; supraclavicular mass; lymph node larger than 2 cm in diameter; persistent enlargement for more than two weeks; no decrease in size after four to six weeks; absence of inflammation; ulceration; failure to respond to antibiotic therapy; or a thyroid mass), the patient should be referred to a head and neck surgeon for urgent evaluation and possible biopsy.
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PMID:Evaluation and management of neck masses in children. 2469 6

Meningococcal infection is among the most devastating diseases. It is rarely seen in Japan. However, several environmental and host factors have been associated with increased risks of Neisseria meningitidis infection. We present a case of invasive N. meningitidis infection that revealed the presence of multiple myeloma. A 55-year-old Japanese man was admitted with fever and altered consciousness. He was sent to the intensive care unit for septic shock and disseminated intravascular coagulation. In addition to standard septic shock and multiple organ failure treatment, polymyxin-B immobilized column direct hemoperfusion was performed. His blood culture was positive for N. meningitidis. The patient gradually improved and was discharged on day 35. We evaluated the risk factors for the development of meningococcal infection. A laboratory examination showed that the patient was negative for human immunodeficiency virus antibody and had a normal total complement function. However, his serum immunoglobulin G level was high, and serum and urine protein electrophoresis detected a monoclonal gammopathy. A bone marrow examination led to the diagnosis of multiple myeloma. Because N. meningitidis bacteria spreads between individuals in close contact through the exchange of oral secretions, droplet precautions and antimicrobial chemoprophylaxis (ciprofloxacin, 500 mg) were implemented to prevent the spread of the meningococcal infection. Sporadic meningococcal infection warrants an evaluation for immunodeficiency and the prevention of secondary infection.
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PMID:[Meningococcal Septicemia Revealing Multiple Myeloma: A Case Report]. 2752 71


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