COVID-19後的免疫負債與病毒再流行：呼吸道融合病毒與人類微小病毒B19

Abstract

2019 年底開始的 COVID-19 爆發，促使包括臺灣與日本在內的東亞國家採取了嚴格的非藥物介入措施（non-pharmaceutical interventions, NPIs），如口罩強制令、社交距離限制及邊境管制等政策。儘管這些措施有效抑制了 SARS-CoV-2 的傳播，也同時降低了其他常見呼吸道病毒的傳播，使原本透過反覆季節性暴露所維持的群體免疫受到影響。由此產生的易感人群累積，即所謂的「免疫負債」（immunity debt），被認為是非藥物介入措施解除後多種呼吸道病毒出現異常大規模再流行的重要驅動因素。 為探討免疫負債對不同呼吸道病毒再流行的影響，本研究以呼吸道融合病毒（Respiratory Syncytial Virus, RSV）感染症及由人類微小病毒 B19（Parvovirus B19）引起的傳染性紅斑（第五病）為研究對象。利用日本與臺灣過去十年間的傳染病監測資料建立傳播模型，其中日本資料包含年齡分層病例資訊。RSV 採用 SIRS（易感–感染–康復–易感）模型，傳染性紅斑則採用 SIR（易感–感染–康復）模型，以描述兩種疾病不同的免疫特性及傳播動態。 模型分析結果顯示，COVID-19 疫情期間非藥物介入措施導致兩種疾病的易感人群皆明顯累積，但其疫情再流行模式存在顯著差異。RSV 在防疫措施放寬後迅速恢復流行，而傳染性紅斑則於數年後才出現延遲且大規模的疫情再流行，顯示免疫特性與傳播週期共同影響疫情恢復的時機與規模。此外，臺灣與日本的 RSV 亦呈現不同的疫情恢復軌跡，反映不同防疫政策及流行病學背景對病毒傳播動態的影響。 本研究支持免疫負債為 COVID-19 後病毒再流行的重要機制之一，並顯示不同病原體因免疫持續時間及傳播特性的差異，可能產生不同的疫情恢復模式，研究結果可作為未來公共衛生防疫策略規劃及地方性傳染病監測的重要參考。

The emergence of COVID-19 in late 2019 prompted East Asian countries, including Taiwan and Japan, to implement stringent non-pharmaceutical interventions (NPIs), such as mandatory masking, social distancing, and border control. While these measures effectively reduced the transmission of SARS-CoV-2, they also suppressed the circulation of other common respiratory viruses that normally maintain population immunity through repeated seasonal exposure. The resulting accumulation of susceptible individuals, referred to as immunity debt, has been proposed as an important driver of the unusually large post-pandemic resurgence of multiple respiratory viruses following the relaxation of NPIs. To investigate the impact of immunity debt on the post-pandemic resurgence of respiratory viruses, this study focused on respiratory syncytial virus (RSV) infection and erythema infectiosum (fifth disease) caused by human parvovirus B19. Surveillance data collected over the past decade from Japan and Taiwan were analyzed to develop compartmental transmission models, with age-stratified case data available for the Japanese surveillance system. An SIRS (Susceptible–Infected–Recovered–Susceptible) compartmental model was developed for RSV, whereas a SIR (Susceptible–Infected–Recovered) compartmental model was used for erythema infectiosum to reflect their distinct immunological characteristics. Model analyses showed that susceptible individuals accumulated substantially for both diseases during the COVID-19 pandemic because of reduced viral transmission; however, their post-pandemic resurgence patterns differed markedly. RSV rapidly resumed circulation following the relaxation of NPIs, whereas erythema infectiosum exhibited a delayed but pronounced resurgence several years later, suggesting that differences in immune characteristics and epidemic periodicity jointly influenced the timing and magnitude of epidemic recovery. In addition, RSV epidemics in Taiwan and Japan followed distinct recovery trajectories, highlighting the influence of different public health policies and epidemiological settings on transmission dynamics. Overall, the findings support immunity debt as an important mechanism underlying post-pandemic viral resurgence while demonstrating that epidemic recovery varies across pathogens according to their immunological characteristics and transmission dynamics. These results provide evidence to inform future public health preparedness and surveillance strategies for endemic infectious diseases.