Unrelated animal viruses share receptors.
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Biomedical subjects
Publications and source records attributed to K Lonberg-Holm.
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Subviral particles ("A particles") were produced from rhinovirus type 2 by treatment with acid and from poliovirus type 2 by incubation at 37 degrees C in a low-ionic-strength buffer. A particles, but not virions, adsorbed to liposomes. It is proposed that these reactions may provide an in vitro model for two early steps of infection.
Attachment, ""tight binding'' and eclipse of radioactive poliovirus 2 (P2) and human rhinovirus 2 (HRV 2) were investigated. The activation energy for attachment of both HRV2 and P2 was about 13 kcal/mol. HRV2 differed from P2 in two respects: the Arrhenius plot for attachment of HRV2 showed a break at 15 to 19 degrees C when the cells were first treated several hours at 0 degrees C, and attachment of HRV2 was inhibited by treatment of cells with metabolic poisons able to reduce cellular ATP by more than 90%. Tight binding was determined by isolation of a specific P2-membrane complex or by loss of EDTA dissociability of HRV2. Tight binding of both viruses was slowed by 0.01 M iodoacetamide but not by 0.02 M F-; F- plus 0.002 M CN- slowed tight binding of HRV2 but not of P2. Eclipse, the irreversible alteration of parental virions, was detected by isolation of cell-associated subviral particles or by loss of cell-associated infectious virus. Eclipse of both viruses is slowed by iodoacetamide or F-. It seems likely that the early steps of infection with picornaviruses may be sensitive to alterations in the cell membrane produced by metabolic inhibitors or by treatment at low temperature.
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HeLa cells infected with radioactive poliovirus type 2 were disrupted with ultrasonic treatment, followed by addition of a non-ionic detergent. Two types of virus particles were found to sediment at 80 to 90% the rate of native virus. The first of these appeared to be a complex of native virus particles and membrane components, since treatment with 0-2% SDS released infectious native particles. The second was non-infectious and its sedimentation rate was not greatly altered by SDS. One hour after infection this non-infectious particle was the major product of cell-mediated eclipse. We have confirmed that 10 to 30 mg-g/ml S-7, a substituted thiopyrimidine, blocks infection of cells by poliovirus in a specific manner. Analysis of cells infected with radioactive poliovirus type 2 in the presence of S-7 showed that the virus particles remained as the complex which can be disrupted with SDS. In addition to blocking cell-mediated eclipse, S-7 stabilizes poliovirus against heat inactivation in vitro at the same concentrations which block infection. This action resembles the effect of 10-2 M-glutathione, which is also known to block cell-mediated eclipse of poliovirus.
The effect of concanavalin A (Con A) on the course of early infection of HeLa cells with purified radioactive human rhinovirus type 2 (HRV-2) or poliovirus type 2 (P-2) has been examined. Several early steps in infection were inhibited before the uncoating of parental virus. Con A, at 100 mug/ml, reduces attachment of virus when added to cells before infection. Con A also detectably slows the normal progression of adsorbed virus to tightly bound forms characterized, in the case of HRV-2, by resistance to elution by EDTA, or in a case of P-2, by isolation of a characteristic virus-membrane complex. When Con A is added together with either virus, it also inhibits cell-mediated eclipse of infectivity and the formation of non-infective subviral particles.