Information has been received from the authors in a published literature article title as stated above that their study extends the current understanding of early immune responses to hepatitis B virus (HBV) in unvaccinated individuals while providing insight into which cytokines/chemokines are induced during a virological challenge in individuals who had already been vaccinated, thereby providing a model for an effective, albeit nonsterilizing, vaccine-induced immune response. All testing was performed on de-identified repository specimens from consented blood and plasma donors and therefore not considered human subjects research. Longitudinally collected acute HBV infection panels were obtained from 3 sources. Authors studied 6 individuals who were identified as having confirmed or probable HBV vaccine breakthrough infections. Based on anti-HBs screening of the first samples of 55 plasma donor panels, authors identified 2 plasma donor (MARRS # 1407USA002393) panels with evidence of probable vaccine breath through infection (ie, the presence of anti-HBs and HBV DNA in the absence of anti-HBc on the first available plasma donation sample, followed by the appearance of HBsAg on subsequent donation-derived samples). These 2 panels had 9 and 26 longitudinal samples. There were 4 additional previously vaccinated whole blood donors who were identified by NAT testing as having HBV vaccine breakthrough infections, as reported elsewhere. These blood donor vaccine breakthrough infection panels had an average of 10 serial samples (range, 8-13) that were at convenient time intervals following HBV DNA detection on index donations. This analysis of the dynamics of viral and serological markers in the context of vaccine-induced pre-existing immunity shows early innate and adaptive immune responses that may be specific to infections that occur despite partial vaccine-induced protection. Also it was reported that this study nonetheless revealed significantly elevated immune responses during acute infection in non vaccinated and vaccinated individuals, and authors demonstrated that although HBV vaccination may not be "sterilizing" in all cases, when breakthrough infections occur they were characterized by earlier immune responses in the context of suppressed viral replication dynamics. In conclusion, this study shows that earlier initiation of immune responses may mediate vaccine-induced protection preventing symptomatic acute and chronic HBV infections in individuals with HBV vaccine breakthrough infections. Authors identified common early induction of several cytokines and chemokines (ide, IP-10, sIL-2Ra., MIP-1B and IL-10) that may play a role in triggering earlier adaptive cellular responses, thus regulating inflammation and inducing anamnestic anti-HB's antibodies to help control viremia. Further studies of viral control and immune response in the context of pre-existing vaccination are needed to fully understand mechanisms underlying vaccine breakthrough infection such as incomplete seroconversion, waning anti-HBs, or prevalence of diverse HBV genotypes. Finally, studies elucidating consequences of vaccine breakthrough infection should be conducted to determine if there is persistence of HBV after breakthrough infection and if these individuals are susceptible to reactivation in the context of immunosuppression as in classically resolved HBV infections. This is one of several reports from the same source (MARRS #1407USA002393). A copy of the published article is attached as further documentation of the patient's experience. Additional information has been requested.