Deletions and duplication in internal inverted repeat sequence of long region/unique sequence of long region [IRL/UL] of herpes simplex virus type-1 [HSV-1] genome are not evidently associated with intracranial and foot-pad pathogenicity in mouse model

The biological properties of three deletion variants [1704, 1705 and 1706] of herpes simplex virus type-1 [HSV-1] strain 17 syn+, were studied by establishing a base line pathogenicity of nine individual plaques from the parental 17 syn+ elite stock. Restriction enzyme analysis of deoxyribonucleic acid [DNA] from each of the nine plaque stocks and intracranial inoculation into three weeks old BALB/c mice showed no difference in the size of fragments and distribution of the sites or their 50% lethal dose [LD[50]] values [plaque forming units [pfu]/mouse] as compared to the parental 17 syn+ stock. Inoculation of the variants into three weeks old BALB/c mice showed that 1705 was not different in pathogenicity from the wild type following intracranial and footpad inoculations. On the other hand variants 1704 and 1706, when compared to the wild type virus were less virulent on intracranial inoculation i.e. the difference in LD[50] values was approximately one log and two logs respectively and both the variants failed to kill any of the animals following footpad inoculation even at the dose of 1x10[7] pfu/mouse. During in vivo replication experiment in the peripheral nervous system of mice, 1704 and 1706 grew very poorly

Latent phenotype analysis of three deletion variants of herpes simplex virus type 1 [HSV-1] in mouse model

Latency analysis of three herpes simplex virus type [HSV-1] strain 17 syn+ deletion variants [1704, 1705 and 1706] showed that they established, maintained and reactivated from latency. The kinetics of reactivation of 1705 and 1706 were similar to the parent HSV-1, 17 syn+, in which reactivation occurred 5-6 days post-explantation, but 1704 reactivated with delayed kinetics i.e. on the 12th day post-explantation. Since 1704 has deleted both copies of the latency associated transcripts [LATs] promoter region and one copy of the LAT coding region in internal inverted repeat sequence of long region [IR[L]], it was concluded that the LATs play a part in latency reactivation of 1704 from dorsal root ganglia [DRG] of spinal cord in mouse model. Restoration of the deleted sequences in the variant 1704 by marker rescue with the wild type BamHIb fragment resulted in a wild type genotype. This virus was designated as 1704R. Latency studies of 1704R revealed that the rate and frequency of reactivation was intermediate between 17 syn+ and 1704, suggesting a secondary undetected mutation affecting latency phenotype. Isolation of 1704LP-, during the same marker rescue experiment in which both copies of promoter region of the LAT are deleted and reactivation of this virus from latency with delayed kinetics confirms that the LATs play a role in reactivation form latency

Prevalence of pathogenic intestinal parasites among pre-school children in Kuri-Sher, Islamabad

The prevalence of intestinal parasites in pre-school children in a rural area near Islamabad was found to be 53.6%. Over all 600 stool samples were examined from both the sexes. The rate was slightly higher in females [56.6%] than in males [49.6%]. The most common parasite was found to be Giardia lamblia and most common round worm was Ascaris lumbricoides. The prevalence of Ascaris lumbriciodes, Ancylostoma duodenale and Hymenolepis nana infestation was found to be increasing with increasing age of the child