An analysis of trends and determinants of health insurance and healthcare utilisation in the Russian population between 2000 and 2004: the 'inverse care law' in action

BACKGROUND: The break-up of the USSR brought considerable disruption to health services in Russia. The uptake of compulsory health insurance rose rapidly after its introduction in 1993. However, by 2000 coverage was still incomplete, especially amongst the disadvantaged. By this time, however, the state health service had become more stable, and the private sector was growing. This paper describes subsequent trends and determinants of healthcare insurance coverage in Russia, and its relationship with health service utilisation, as well as the role of the private sector. METHODS: Data were from the Russia Longitudinal Monitoring Survey, an annual household panel survey (2000-4) from 38 centres across the Russian Federation. Annual trends in insurance coverage were measured (2000-4). Cross-sectional multivariate analyses of the determinants of health insurance and its relationship with health care utilisation were performed in working-age people (18-59 years) using 2004 data. RESULTS: Between 2000 and 2004, coverage by the compulsory insurance scheme increased from 88% to 94% of adults; however 10% of working-age men remained uninsured. Compulsory health insurance coverage was lower amongst the poor, unemployed, unhealthy and people outside the main cities. The uninsured were less likely to seek medical help for new health problems. 3% of respondents had supplementary (private) insurance, and rising utilisation of private healthcare was greatest amongst the more educated and wealthy. CONCLUSION: Despite high population insurance coverage, a multiply disadvantaged uninsured minority remains, with low utilisation of health services. Universal insurance could therefore increase access, and potentially contribute to reducing avoidable healthcare-related mortality. Meanwhile, the socioeconomically advantaged are turning increasingly to a growing private sector

RNA-Seq analysis of chikungunya virus infection and identification of granzyme A as a major promoter of arthritic inflammation

Chikungunya virus (CHIKV) is an arthritogenic alphavirus causing epidemics of acute and chronic arthritic disease. Herein we describe a comprehensive RNA-Seq analysis of feet and lymph nodes at peak viraemia (day 2 post infection), acute arthritis (day 7) and chronic disease (day 30) in the CHIKV adult wild-type mouse model. Genes previously shown to be up-regulated in CHIKV patients were also up-regulated in the mouse model. CHIKV sequence information was also obtained with up to ≈8% of the reads mapping to the viral genome; however, no adaptive viral genome changes were apparent. Although day 2, 7 and 30 represent distinct stages of infection and disease, there was a pronounced overlap in up-regulated host genes and pathways. Type I interferon response genes (IRGs) represented up to ≈50% of up-regulated genes, even after loss of type I interferon induction on days 7 and 30. Bioinformatic analyses suggested a number of interferon response factors were primarily responsible for maintaining type I IRG induction. A group of genes prominent in the RNA-Seq analysis and hitherto unexplored in viral arthropathies were granzymes A, B and K. Granzyme Aand to a lesser extent granzyme K, but not granzyme B, mice showed a pronounced reduction in foot swelling and arthritis, with analysis of granzyme Amice showing no reductions in viral loads but reduced NK and T cell infiltrates post CHIKV infection. Treatment with Serpinb6b, a granzyme A inhibitor, also reduced arthritic inflammation in wild-type mice. In non-human primates circulating granzyme A levels were elevated after CHIKV infection, with the increase correlating with viral load. Elevated granzyme A levels were also seen in a small cohort of human CHIKV patients. Taken together these results suggest granzyme A is an important driver of arthritic inflammation and a potential target for therapy. Trial Registration: ClinicalTrials.gov NCT0028129