No abstract
Although polyomavirus JC (JCV) is the proven pathogen of progressive multifocal leukoencephalopathy, the fatal demyelinating disease, this virus is ubiquitous as a usually harmless symbiote among human beings. JCV propagates in the adult kidney and excretes its progeny in urine, from which JCV DNA can readily be recovered. The main mode of transmission of JCV is from parents to children through long cohabitation. In this study, we collected a substantial number of urine samples from native inhabitants of 34 countries in Europe, Africa, and Asia. A 610-bp segment of JCV DNA was amplified from each urine sample, and its DNA sequence was determined. A worldwide phylogenetic tree subsequently constructed revealed the presence of nine subtypes including minor ones. Five subtypes (EU, Af2, B1, SC, and CY) occupied rather large territories that overlapped with each other at their boundaries. The entire Europe, northern Africa, and western Asia were the domain of EU, whereas the domain of Af2 included nearly all of Africa and southwestern Asia all the way to the northeastern edge of India. Partially overlapping domains in Asia were occupied by subtypes B1, SC, and CY. Of particular interest was the recovery of JCV subtypes in a pocket or pockets that were separated by great geographic distances from the main domains of those subtypes. Certain of these pockets can readily be explained by recent migrations of human populations carrying these subtypes. Overall, it appears that JCV genotyping promises to reveal previously unknown human migration routes: ancient as well as recent.
In 2001, Myanmar (Burma) had its largest outbreak of dengue—15,361 reported cases of dengue hemorrhagic fever/dengue shock syndrome (DHF/DSS), including 192 deaths. That year, 95% of dengue viruses isolated from patients were serotype 1 viruses belonging to two lineages that had diverged from an earlier, now extinct, lineage sometime before 1998. The ratio of DHF to DSS cases in 2001 was not significantly different from that in 2000, when 1,816 cases of DHF/DSS were reported and dengue 1 also was the most frequently isolated serotype. However, the 2001 ratio was significantly higher than that in 1998 (also an outbreak year) and in 1999, when all four serotypes were detected and serotypes 1, 2, and 3 were recovered in similar numbers. The large number of clinical cases in 2001 may have been due, in part, to a preponderance of infections with dengue 1 viruses.
Extensive complement activation precedes onset of shock in dengue patients and complement "split products" C3a and C5a could be responsible, directly or indirectly, for the increased vascular permeability and disseminated intravascular coagulation which characterises dengue haemorrhagic fever (DHF) dengue shock syndrome (DSS). As IgG subclasses vary in their capacity to activate the classical complement pathway after combining with antigen, we have used an indirect enzyme linked immunosorbent assay (ELISA) to assess levels of IgG1-4 against each dengue serotype in acute and convalescent sera from patients with disease of varying severity. Acute phase sera from patients with dengue haemorrhagic fever (DHF) or dengue shock syndrome (DSS) contained higher levels of anti-dengue antibodies of the IgG1, complement fixing, subclass than similar sera from dengue fever (DF) patients. Conversely, acute phase sera from DHF and DSS patients contained lower levels of anti-dengue antibodies of the poor complement activating IgG2 subclass than acute phase sera from DF patients. No significant differences were detected between the levels of anti-dengue IgG3 and IgG4 antibody in acute phase sera from DF, DHF, and DSS patients. With the exception of levels of anti-dengue IgG2 antibody from DHF patients which were lower than those from DF and DSS patients, levels of anti-dengue IgG1, IgG2, IgG3, and IgG4 were similar in convalescent sera from all patients. These results provide a possible explanation for the activation of the serum complement system which precedes onset of shock in severe dengue infections.
During 1984, 1548 children were admitted to the Yangon [Rangoon] Children's Hospital in Myanmar [Burma] with haemorrhagic fever. No evidence of recent dengue infection was found in 577 of the 803 children from whom paired sera were obtained, raising the possibility of reappearance of Chikungunya virus infection in Myanmar. An enzyme-linked immunosorbent assay (ELISA) for the detection of anti-Chikungunya virus immunoglobulin M (IgM) antibody was prepared and standardized using only reagents which are commercially available or which could be prepared without the use of sophisticated equipment. While there was 90% agreement between haemagglutination inhibition (HI) tests and the IgM ELISA in the diagnosis of acute Chikungunya virus infections, 12 additional patients with stationary anti-Chikungunya virus HI antibody titres could be identified as having acute Chikungunya infections using the ELISA. Furthermore, the ELISA could identify twice as many patients (31/103) at the time of admission to hospital as the HI test (15/103). There was no false positive IgM reaction with the ELISA which could be attributed to the presence of rheumatoid factor. Using the test, 103 of a sample of 163 children who presented to the Yangon Children's Hospital with fever/haemorrhagic fever were diagnosed as Chikungunya patients, 4 had possible dual Chikungunya and dengue infections, 16 had dengue, 30 had neither Chikungunya nor dengue infections, and a definitive diagnosis could not be made for 10 patients. Routine use of the ELISA would alert authorities to future outbreaks of Chikungunya virus infection and avoid admission to hospital of patients with a non-life-threatening viral disease.
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