The molecular epidemiology of molluscum contagiosum virus (MCV) infections was investigated by restriction endonuclease analysis of the genomes of 222 separate isolates collected from 147 patients living in Germany (33 patients), Hong Kong (6 patients), and Scotland (108 patients). MCV type 1 (MCV-1) caused 96.6% of the infections, and MCV type 2 (MCV-2) caused 3.4%. However, isolates from four of the 142 MCV-1-infected patients and two of the five MCV-2-infected patients showed minor differences in their DNA restriction patterns because of the loss of a single or very few recognition sites for the enzymes used. No genome variations were detected amongst isolates collected from different sites or on several occasions from individual patients or from closely related patients. Southern blot hybridization revealed a high level of relatedness between MCV-1 and 2. No differences were seen in the appearance or anatomical localization of lesions caused by either virus type. In particular, there was no preferred genital localization for MCV-2 infections.

Virions of molluscum contagiosum virus (MCV), a member of the poxviridae, were isolated directly from lesions of individual patients and characterized by restriction enzyme analysis. The comparative analysis of the cleavage patterns and Southern blot hybridization of 14 independently isolated virus samples revealed that MCV isolates can be classified into two different types. The majority of MCV isolated from clinically typical skin lesions (13 of 14) showed similar DNA cleavage patterns and were termed MCV type 1, whereas one isolate derived from a vaginal lesion showed a completely different DNA cleavage pattern and therefore was termed MCV type 2. For detailed investigation of the viral genome, a defined gene library of MCV DNA sequences was established. The Bam HI DNA fragments of the viral genome of MCV type 1 prototype isolate 1/80 was inserted into the bacterial plasmid vector pAT153. With the exception of terminal fragments (fragments A and B) of the viral genome, all other DNA fragments were cloned. All cloned Bam HI DNA fragments were individually identified by digestion of the recombinant plasmid DNA with different restriction enzymes and screened by hybridization of plasmid DNA to viral DNA.

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Disoxaril , 5-[7-[4(4,5 -dihydro-2-oxazolyl)phenoxy] heptyl]-3-methylisoxazole, inhibits the replication of several picornaviruses (Otto et al., Antimicrob. Ag. Chemother. 27 (1985) 883-886). Measurements of viral RNA synthesis and electron microscopy showed that disoxaril inhibits the replication of poliovirus types 1 and 2 in HeLa cells prior to uncoating by stabilizing the virus capsid: The arrival of viral RNA for new RNA synthesis was inhibited completely only when the inocula were preincubated with disoxaril for 15 min at 37°C at 0.3 Ilg disoxarillml for poliovirus type 1 and 0.03 ug disoxarillml for poliovirus type 2. Simultaneous addition of the compound and virus resulted in reduced inhibition of viral RNA synthesis. The inhibitory effect of the compound could be partially reversed up to 25 min p.i. if the compound was eluted from the cells. Disoxaril pretreated poliovirus was not inhibited from entering HeLa cells (entry by receptor-mediated endocytosis via coated pits and vesicles into endosomes) (d.