HCV epidemic in North America peaked between 1940 and 1965 with medical procedures likely source of most infections

Most baby boomers infected in hospital and by reused medical syringes, not injecting drug use or risky sex
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The spread of hepatitis C virus (HCV) in North America peaked between 1940 and 1965, according to research published in Lancet Infectious Diseases. The investigators attribute the rapid spread of the infection to hospital transmissions and reuse of medical injecting equipment rather than risky behaviours such as injecting drugs, unsafe tattooing and unprotected sex.

“Based on our results, the oldest members of the demographic cohort with the highest burden of hepatitis C virus (the baby boomers) were roughly five years of age around the peak of the spreads of genotype 1a in North America in 1950,” comment the authors. “Thus, it is unlikely that past sporadic risky behaviour (experimentation with injecting drug use, unsafe tattooing, high risk sex, travel to endemic areas) was the dominant route of transmission in this group.” The researchers hope their findings will help de-stigmatise HCV infection in the baby boomer generation and encourage more patients to access testing and potentially life-saving treatment.

Up to 6 million individuals in North America are infected with HCV. Approximately three-quarters of these infections involve patients born between 1945 and 1965, the baby boomer generation. Previous studies have identified infected blood products and experimentation with injecting drug use as the main factors driving the spread of HCV in this age group.

Glossary

phylogenetic analysis

The comparison of the genetic sequence of the virus in different individuals in order to determine the likelihood that two or more samples are related. This involves creating a hypothetical diagram (known as a phylogenetic tree) that estimates how closely related the samples of HIV taken from different individuals are. Phylogenetic analysis is not a reliable way to prove that one individual has infected another, but may identify transmission clusters, which can be useful for public health interventions.

genes

Genes are instruction manuals for our bodies. They determine characteristics like our eye and hair colour. Every human has a set of around 20,000 genes. We get one copy of each gene from each of our parents. Genes can also play a part in our health and may affect our risk of developing some health condition.

strain

A variant characterised by a specific genotype.

 

gene

A unit of heredity, that determines a specific feature of the shape of a living organism. This genetic element is a sequence of DNA (or RNA, for viruses), located in a very specific place (locus) of a chromosome.

epidemiology

The study of the causes of a disease, its distribution within a population, and measures for control and prevention. Epidemiology focuses on groups rather than individuals.

However, how and when HCV reached such high prevalence in the 1945-65 birth cohort remains unclear. A team of investigators therefore analysed 45,316 sequences of HCV genotype 1a – by far the most common HCV strain in North America. Using a technique called phylogenetic analysis they focused on five HCV genes to reconstruct the dynamics of the HCV epidemic in North America.

Analysis of all five gene regions suggested that the greatest expansion of the epidemic occurred between 1940 and 1965. The massive growth of the epidemic had subsided by 1965 and plateaued between 1965 and 1989. There was a drop in the number of new infections in the 1990s followed by a modest increase from 2000.

Analysis of separate genes revealed a variation in the period of greatest growth, ranging from circa 1940 for NS2, to 1965 for NS4B. Overall, phylogenetic analysis most strongly suggested that the period 1948 to 1963 saw the biggest expansion of the HCV epidemic.

“In sum, our phylogenetic analyses strongly suggest that the hepatitis C genotype 1a epidemic in North America had already attained the height of its distribution by 1960,” write the authors. “These analyses suggest the period of greatest increase in North America was substantially earlier than previously suggested.”

The early expansion of the epidemic coincided with the increase in the number of medical procedures conducted during World War Two and its immediate aftermath, a period when injection and blood transfusion technologies were still in their infancy.

Before 1950, injecting technology was characterised by the use of glass and metal syringes, which were sterilised manually and reused. These were phased out and replaced by disposable syringes between 1950 and 1960 and after 1960 the reuse of syringes was greatly reduced in North America. The period 1920 to 1960 also saw the expansion of recreational drug use and needle sharing, which peaked in the late 1960s.

The spread of HCV during the plateau period – 1965 to 1989 – was likely due to transfusion with contaminated blood products. Rigorous screening was only introduced in 1992, and consistent with this innovation, the investigators found a reduction in the rate of new infections after 1990.

The slight up-turn in infections after 2000 is consistent with epidemiological evidence of increases in HCV infections among young injecting drug users and also HIV-positive men who have sex with men. 

“Our data indicate that the rapid and large-scale expansion of hepatitis C virus transmission in North America was coincident with increases in medical procedures that began after World War Two…and not only the rise in injecting drug use, which peaked much later in North America in the late 1960s,” conclude the authors. “The prevailing view that the North American epidemic is predominately attributable to past sporadic risky behaviours is not supported by our data.”

The investigators hope their findings will help reduce the stigma associated with HCV screening, potentially increasing the number of patients presenting for care and effective treatment.

References

Joy JB et al. The spread of hepatitis C virus genotype 1a in North America: a retrospective phylogenetic study. Lancet Infectious Diseases. Online edition, dx.doi.org/10.1016/S1437-3099(16)00124-9.