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Biomedical subjects

I Tamm

Publications and source records attributed to I Tamm.

144 records · Page 8Linked to original sources
PubMed1969

Formation of viral ribonucleic acid and virus in cells that are permissive or nonpermissive for murine encephalomyelitis virus (GDVII).

GDVII virus growth in BHK-21 cells, a permissive host for the virus, resembled productive infections with other picornaviruses. Virus yields ranged from 100 to 600 plaque-forming units (PFU)/cell. Virus replication in HeLa cells, a nonpermissive host for GDVII virus, was characterized by virus yields of only 0.1 to 5 PFU/cell. Similar low yields of virus have been obtained from HeLa cells at all multiplicities of input up to 6,000 per cell. The progeny particles from HeLa cells were, like the infecting particles, restricted in the HeLa cell host. Despite the great difference in final yields of virus from BHK-21 and HeLa cells, the times when maximal yields were reached were similar. GDVII virus stock grown in BHK-21 cells was designated HeLa(-). A variant of GDVII virus which is capable of extensive growth in HeLa cells was obtained. This variant, designated HeLa(+) GDVII virus, was passaged serially in HeLa cells. Virus yields of 50 to 150 infective virus particles per cell were obtained from infection of HeLa cells with HeLa(+) GDVII virus. The major species of HeLa(+) virus-specific ribonucleic acid (RNA) produced was single stranded and sedimented with an S value of 35S. The rate of accumulation of HeLa(+) virus-specific RNA in HeLa cell cultures was about four times that of HeLa(-) RNA. The amount of virus-specific HeLa(+) RNA formed in HeLa cells was several-fold greater than that of HeLa(-) RNA. With HeLa(-) parent GDVII virus undergoing productive replication in BHK-21 cells or abortive replication in HeLa cells, the major species of virus-specific RNA produced was single stranded and sedimented with an approximate S value of 35S. The amount of HeLa(-) virus-specific RNA extracted from BHK-21 cells was several-fold greater than the amount obtained from HeLa cells.

Centrifugation, Density Gradient↗
PubMed1966

Inhibition of enterovirus cytopathic effects by 2-(alpha-hydroxybenzyl)-benzimidazole.

Bablanian, Rostom (The Rockefeller University, New York, N.Y.), Hans J. Eggers, and Igor Tamm. Inhibition of enterovirus cytopathic effects by 2-(alpha-hydroxybenzyl)-benzimidazole. J. Bacteriol. 91:1289-1294. 1966.-2-(alpha-Hydroxybenzyl)-benzimidazole (HBB), a specific inhibitor of enterovirus multiplication, markedly delayed the development of cytopathological changes induced by echovirus 12 or coxsackievirus B4 in monkey kidney cells, but did not prevent the ultimate degeneration of infected cells, even though virus multiplication was inhibited. The study of the development of viral cytopathic effects was facilitated by the use of antiviral immune serum, which restricted the infection to those cells which became infected by the inoculated virus and thereby established single-cycle conditions. With echovirus 12 and coxsackievirus B4 not all cells could be infected initially, even when cultures were inoculated at input multiplicities in excess of 100 plaque-forming units per cell.

Animals↗
PubMed1965

Chemical approaches to selective inhibition of viral multiplication.

There are more than 300 immunological types of viruses that infect man, but most are members of only eight major groups, each group characterized by distinguishing physical and chemical features. Chemical inhibitors have been discovered which are selectively directed against members of individual groups of viruses. These inhibitors interfere with virus-specific processes and have no effects on host cell metabolism at concentrations sufficient to prevent or stop virus multiplication. The biochemical basis of such selective action is understood in some cases. In addition, synthetic chemicals and biological products are known that inhibit members of several groups of viruses. The basis of their selective action is not clear.

Antiviral Agents↗
PubMedDate not supplied

Pleural effusion due to Histoplasma capsulatum and idiopathic CD4 lymphocytopenia.

Acute histoplasmosis is usually a benign, self-limited infection in endemic areas. Since protection against Histoplasma capsulatum infection requires specific, cell-mediated immunity, histoplasmosis is well documented in patients with acquired T cell deficiencies e.g. due to HIV infection. We report here for the first time a case of pleural effusion due to H. capsulatum infection in a patient with idiopathic CD4 lymphocytopenia (ICL). A 25-year-old woman presented with chest pain, dyspnea on exertion and a moderate weight loss. Chest X-ray showed a large left pleural effusion, and thoracentesis yielded an exudate. Histologic examination of pleural biopsies identified H. capsulatum. Laboratory tests revealed lymphocytopenia with low CD4+ T cell counts (<100/microl) and a decreased CD4/CD8 ratio. Serology, including HIV, was repeatedly negative. The diagnosis of pleural effusion due to H. capsulatum infection in a patient with idiophatic ICL was established. There was no evidence of any other opportunistic infection. Treatment with itraconazole was initiated and pleural effusion resolved within 2 weeks of treatment. Moreover, the patient was found to have idiopathic thrombocytopenic purpura, as confirmed by the detection of autoantibodies against thrombocytes. In a 1-year follow-up, the patient remained asymptomatic without relapse or any new infection. Treatment with itraconazole was given for 12 months. Because of persistent CD4+ T cell counts below 100/microl, prophylactic antibiotic treatment is continued.

Adult↗
PubMedDate not supplied

Dacarbazine and interferon alpha for stage IV malignant melanoma.

Based on encouraging reports of improved response rates with the use of dacarbazine (DTIC) in combination with recombinant interferon alpha-2a (rIFN-alpha-2a) in patients with metastatic malignant melanoma, we conducted a phase II study to determine the efficacy and feasibility of this treatment regimen. 31 patients were treated with an induction dose of rIFN-alpha-2a at 15 MIU/ m2 intravenously (i.v.) daily for 5 days per week for 3 consecutive weeks followed by a continuous maintenance dose of 10 MIU/m2 subcutaneously (s.c.) given 3 days per week; starting on day 22, in conjunction with rIFN-alpha-2a s.c., DTIC was started at a dose of 200 mg/m2 i.v. for 5 continuous days completing a 28-day cycle. Therapy was continued until progression was evidenced. Of the 29 evaluable patients, 7 (24.1%) achieved an objective response (complete plus partial remission) with the highest responses occurring in those patients assessed with pulmonary metastases. The median duration to treatment failure was 2.6 months, while the median survival was 6.9 months. Our data reveal that using rIFN-alpha-2a plus DTIC in combination does not yield better results than those achieved when using DTIC alone. However, 3 of the 7 responders experienced long-term survival ranging up to 42 months. Whether this benefit is achieved by the addition of rIFN-alpha-2a can only be answered by large randomized clinical trials. Conflicting results with some of the current literature are discussed.

Adult↗