In a groundbreaking study from March 2023, the University of Parma sheds light on the intricate world of chronic hepatitis B, revealing a crucial link between mitochondrial dysfunction, oxidative stress, and compromised CD8 T cells. These cells, vital in fighting the hepatitis B virus, suffer increased DNA damage due to rising levels of reactive oxygen species (ROS). The study emphasizes CD38-mediated NAD+ depletion as a key player in CD8 T cell dysfunction, suggesting potential remedies through NMN supplementation and CD38 inhibition. With chronic hepatitis B presenting significant global health risks, this exploration into T-cell dysfunction opens avenues for intervention, presenting NMN as a beacon of hope for revitalizing immune responses against this pervasive viral threat.

Chronic hepatitis B, a global health concern, involves the HBV virus spreading through various transmission routes. The study uncovers a concerning connection between mitochondrial dysfunction-induced oxidative stress and specific CD8 T cells in chronic HBV patients. Increased ROS levels due to mitochondrial dysfunction lead to heightened DNA damage in CD8 T cells, critical lymphocytes combating the HBV virus. The study attributes this to accelerated NAD+ consumption by CD38, suggesting that NMN supplementation and CD38 inhibition could restore CD8 T cell function.

Globally, chronic hepatitis B results in 1.5 million new HBV infections and 296 million chronic infections, causing 820,000 deaths annually. In China, with a 6.1% prevalence of HBV infection in 2016, chronic HBV infections reached 86 million. The core of chronic hepatitis B development lies in dysfunctional CD8 T cells, crucial for combating the HBV virus. Acute infections exhibit activated CD8 T cells, while chronic infections lack detectable CD8 T cells due to T-cell exhaustion, giving the virus a survival advantage.

Researchers studied 69 patients with chronic active hepatitis B, 12 recovered from acute HBV infection, and 15 healthy subjects, comparing their CD8 T cells. Dysfunction characterized by metabolic disruption and increased DNA damage during chronic HBV infection resulted from NAD+ depletion, especially through excessive CD38 consumption.

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To assess the impact of NMN supplementation and CD38 inhibition, researchers explored their effects on lymphocyte cultures from chronic hepatitis B patients. NMN repaired DNA damage, restored CD8 T cell function, and improved cytokine production, indicating enhanced antiviral function.

The study also examined CD38 inhibition on acetylation in HBV-specific CD8 T cells, showing parallels with NAD+ supplementation. The combined action of NMN and a CD38 inhibitor displayed trends of telomere lengthening and reduced PD1 expression.

Previous research highlights the correlation between liver injuries and reduced NAD+ levels. NMN's protective effects on alcohol-induced liver damage and non-alcoholic fatty liver disease underscore its crucial role in rebuilding T-cell antiviral capabilities and liver health in chronic hepatitis B.