Hemophilia patients more likely to be infected with SENV: Study
Virus detected in more than half of patients with hemophilia A
People with hemophilia are more likely to be infected with the SEN virus (SENV), which is associated with blood transfusion hepatitis, or liver inflammation, than healthy people, a study in Iran suggests.
The virus was detected in more than half of patients with hemophilia A and most commonly in those with more severe disease.
“Our findings highlight the importance of continuous monitoring and follow-up of high-risk groups in relation to blood-borne pathogens, providing reassurance about the ongoing efforts in the field,” the researchers wrote.
The study, “Investigation of SEN virus prevalence in hemophilia patients,” was published in New Microbes and New Infections.
Hemophilia is mainly caused by mutations in genes that provide instructions for producing proteins essential for blood clotting, called blood clotting factors, that prevent excessive bleeding. People with hemophilia produce either a faulty version of a clotting factor, low levels of it, or none at all.
The main treatments for hemophilia are factor replacement therapies, which involve supplying the patient a version of the missing clotting factor. Because these factors are commonly obtained from donor blood, there’s a risk of contamination with blood-borne pathogens, including SENV.
Analyzing prevalence of SENV in hemophilia
Here, a team led by researchers at the Birjand University of Medical Sciences in Iran analyzed the prevalence of SENV and related complications in people with hemophilia. The study included 135 participants, 80 with hemophilia and 55 healthy people. The hemophilia patients were predominantly male (93.7%) and had a mean age of 27.4. The healthy participants were mainly female (63.6%) and had a mean age of 41.6. Most patients (86.3%) had hemophilia A, followed by hemophilia B (6.3%).
The SENV virus was detected in 58 participants (43%), with a significantly higher prevalence among those with hemophilia than healthy people, 58.8% versus 20%. These results underscore a “potentially heightened susceptibility to SENV infection among hemophilic individuals,” the researchers wrote.
The virus wasn’t detected in any participant with hemophilia B, but 65.2% of hemophilia A patients were positive for it.
Those with severe hemophilia A, meaning levels of clotting factor VIII below 1% of normal, had a higher prevalence of SENV (69%), followed by patients with moderate disease (65.8%; patients with FVIII levels between 1%-5% of normal). The virus wasn’t detected in patients with mild hemophilia A (FVIII levels between 5%-10% of normal).
SENV-positive participants were generally younger and had significantly higher levels of the liver enzyme aspartate transaminase (AST), a marker of possible liver damage.
SENV-H and SENV-D are the most common types of the virus. In the study, type D was the most frequently detected (60.3%), followed by SENV-H (39.7%). Coinfection with both SENV-H and SENV-D was seen in 19% of participants.
Clarifying the “immune signature associated with SENV infection” is important for a better understanding of the virus’s “pathogenesis and potential clinical implications,” wrote the researchers, who noted doing so may shed light on possible preventive and therapeutic approaches for “managing infections in high-risk and general populations.” They said future research should include a larger sample size to “enhance the statistical power and generalizability of the results.”
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