Deoxyribonucleic Acid Replication in Simian Virus 40-Infected Cells IV. Two Different Requirements for Protein Synthesis During Simian Virus 40 Deoxyribonucleic Acid Replication

The replication of simian virus 40 (SV40) deoxyribonucleic acid (DNA) was inhibited by 99% 2 hr after the addition of cycloheximide to SV40-infected primary African green monkey kidney cells. The levels of 25S (replicating) and 21S (mature) SV40 DNA synthesized after cycloheximide treatment were always lower than those observed in an infected untreated control culture. This is consistent with a requirement for a protein(s) or for protein synthesis at the initiation step in SV40 DNA replication. The relative proportion of 25S DNA as compared with 21S viral DNA increased with increasing time after cycloheximide treatment. Removal of cycloheximide from inhibited cultures allowed the recovery of viral DNA synthesis to normal levels within 3 hr. During the recovery period, the ratio of 25S DNA to 21S DNA was 10 times higher than that observed after a 30-min pulse with (3)H-thymidine with an infected untreated control culture. The accumulation of 25S replicating SV40 DNA during cycloheximide inhibition or shortly after its removal is interpreted to mean that a protein(s) or protein synthesis is required to convert the 25S replicating DNA to 21S mature viral DNA. Further evidence of a requirement for protein synthesis in the 25S to 21S conversion was obtained by comparing the rate of this conversion in growing and resting cells. The conversion of 25S DNA to 21S DNA took place at a faster rate in infected growing cells than in infected confluent monolayer cultures. A temperature-sensitive SV40 coat protein mutation (large-plaque SV40) had no effect on the replication of SV40 DNA at the nonpermissive temperature.     

Experimental allergic encephalomyelitis in congenic strains of mice

Inbred mice and lines congenic to them for the major histocompatibility complex were similar in susceptibility to EAE except for moderate differences in two pairs. TheH-2 haplotypesq, s, andb occurred in inbred strains and in congenic lines of high, medium, or low susceptibility. It is concluded that the major histocompatibility complex does not control susceptibility to EAE in mice. Furthermore, the low susceptibility of DBA/1J mice was not enhanced by poly A-U.     

The effect of unipolar positively ionized air on the course of coccidioidomycosis in mice

The course of coccidioidomycosis produced in mice by intranasal administration of arthrospores of COCCIDIOIDES IMMITIS was adversely affected by exposure of the animals to air containing 3–4 × 10⁵ positive ions/cm³. A significant number of mice became ill earlier than controls and the cumulative mortality among iontreated animals was higher throughout the 30-day period of observation (difference significant at the 97.5 level by chi-square analysis).The mechanism responsible for this effect is as yet unknown.

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Zusammenfassung Der Verlauf der Coccidioidomykose bei Mäusen, die durch intranasale Verabreichung von COCCIDIOIDES IMMITIS erzeugt wurde, wurde gegensinnig beeinflusst, wenn die Tiere einer Luft mit 3–4 × 10⁵ positiven Ionen/m³ exponiert wurden. Eine signifikante Zahl Mäuse wurde früher krank als die Kontrollen und die kumulative Mortalität der ionen-behandelten Tiere war höher während der 30-tägigen Beobachtungsperiode. Der Wirkungsmechanismus ist noch unbekannt.

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Resume L'évolution de la coccidioïdomycose déclenchée chez des souris par l'application intranasale de COCCIDIOIDES IMMITIS fut influencée de façon contradictoire lorsque les animaux étaient exposés à un air chargé de 3 à 4 × 10⁵ ions positifs par m³. Un nombre significatif de souris furent atteintes du mal plus rapidement que celles servant de contrôle. De même,la mortalité cumulée des animaux traîtés par de l'air ionisé fut plus élevée durant les 30 jours que dura l'essai. Le mécanisme auquel cet effet doit être attribué n'est pas connu jusqu'ici.

     

Mechanism by Which Fiber Antigen Inhibits Multiplication of Type 5 Adenovirus

Purified fiber antigen of type 5 adenovirus inhibited the multiplication of type 5 adenovirus by 50% when 35 mug of fiber antigen protein was added to 10(6) KB cells in suspension culture. Although the fiber antigen reduced the number of virions adsorbed per cell when a multiplicity of infection of 50,000 plaque-forming units (PFU)/cell was employed, the number of cells infected was not diminished under these conditions. If a low multiplicity of infection (1.1 PFU/cell) was used, viral adsorption was not detectably decreased. The fiber antigen did not reduce the capability of virions to liberate their viral deoxyribonucleic acid (DNA). The biosyntheses of DNA, ribonucleic acid (RNA), and protein were blocked about 20 to 25 hr after the addition of fiber antigen to cultures of uninfected or type 5 adenovirus-infected KB cells. Most of the fiber antigen protein became cell-associated between 22 and 36 hr after it was added to cells. The hexon antigen neither inhibited viral multiplication nor blocked the biosynthesis of DNA, RNA, or protein. Moreover, the hexon did not attach to KB cells. The profound effects of the fiber antigen were not due to the induction of an interferon-like substance, for actinomycin D did not reduce the ability of the fiber to inhibit multiplication of type 1 poliovirus.