Вирусные взаимодействия
Feb. 8th, 2025 10:29 pm![[personal profile]](https://www.dreamwidth.org/img/silk/identity/user.png){kind=small}
chuka_lisDisturbed respiratory viral ecology by COVID-19 pandemic reveals the pivotal role of Influenza in virus-virus interaction network
Concurrent epidemics of respiratory viruses provide avenues for intricate virus-virus interactions, yet how molecular-level viral interactions patterns shape viral ecology and epidemic dynamics remain enigmatic. Here, we present real-world virus crosstalk by comprehensively analyzing diagnostic data from a large cohort (37,415 respiratory illness cases pre-COVID-19 pandemic, 22,239 cases thereafter), mainly infants/toddlers, sourced from the same local hospital. Such high-risk group cohort allowed us to examine consistent coinfections among 7 respiratory viruses, despite under an overall reduced infection rates due to COVID-19 disruption. We explored drivers of stable ecosystem and identified a directional virus-virus interaction network between influenza and other respiratory viruses. Monthly prevalence patterns analysis of individual virus revealed IAV positively interacted with RSV, characterized by synchronous seasonality (ρ= 0.67). Conversely, IAV negatively interacted with HPIV3, marked by asynchronous seasonality (ρ= -0.56). Sequential/simultaneous coinfection experiments further confirmed two viruses could contact in the same cell but show distinct coinfection outcomes, such as IAV significantly augmented RSV infection but inhibited HPIV3. We further demonstrated coinfection with IAV and RSV led to exacerbated lung damage in mice, while were associated with aggravated disease outcomes among children. Post-COVID-19, we observed a notable suppression in the spread of respiratory viruses, with a particularly sharp decline in influenza. This reduced influenza activity disrupted virus interactions between influenza and other respiratory viruses, driving the concurrent resurgence of other respiratory viruses. When influenza gradually returns to circulation, the interactions could be reinstated, shaping respiratory virus circulations in a predictable and typical pattern. These findings underscore the pivotal role of influenza in directional interplays among respiratory viruses that shape viral ecology.
Concurrent epidemics of respiratory viruses provide avenues for intricate virus-virus interactions, yet how molecular-level viral interactions patterns shape viral ecology and epidemic dynamics remain enigmatic. Here, we present real-world virus crosstalk by comprehensively analyzing diagnostic data from a large cohort (37,415 respiratory illness cases pre-COVID-19 pandemic, 22,239 cases thereafter), mainly infants/toddlers, sourced from the same local hospital. Such high-risk group cohort allowed us to examine consistent coinfections among 7 respiratory viruses, despite under an overall reduced infection rates due to COVID-19 disruption. We explored drivers of stable ecosystem and identified a directional virus-virus interaction network between influenza and other respiratory viruses. Monthly prevalence patterns analysis of individual virus revealed IAV positively interacted with RSV, characterized by synchronous seasonality (ρ= 0.67). Conversely, IAV negatively interacted with HPIV3, marked by asynchronous seasonality (ρ= -0.56). Sequential/simultaneous coinfection experiments further confirmed two viruses could contact in the same cell but show distinct coinfection outcomes, such as IAV significantly augmented RSV infection but inhibited HPIV3. We further demonstrated coinfection with IAV and RSV led to exacerbated lung damage in mice, while were associated with aggravated disease outcomes among children. Post-COVID-19, we observed a notable suppression in the spread of respiratory viruses, with a particularly sharp decline in influenza. This reduced influenza activity disrupted virus interactions between influenza and other respiratory viruses, driving the concurrent resurgence of other respiratory viruses. When influenza gradually returns to circulation, the interactions could be reinstated, shaping respiratory virus circulations in a predictable and typical pattern. These findings underscore the pivotal role of influenza in directional interplays among respiratory viruses that shape viral ecology.
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no subject
Date: 2025-02-10 07:08 am (UTC)это несколько двояко.
если человек не болеет, значит у него хороший иммунитет (обычно под этим предполагается -врожденный, неспецифический, который просто не пускает возбудителя, абортивные инфекции). если заболел- значит, иммунитет оказался "слабее", чем микроорганизм. а раз слабее, и уже подвергся атаке- организм ослабел еще больше. стал более уязвим и для чего-то другого, потому что на борьбу был оттянут ресурс.
Большинство людей- болеет. не болеют единицы.
так что для людей (большинства) характерно именно то, что они подхватывают инфекции, что их иммунитет не так уж хорош.
Но бывают и парадоксальные ситуации, когда добавочная инфекция помогает победить имеющуюся хроническую, или новообразование, или аутоиммунное заболевание, или еще что- это в случаях когда предыдущее состояние (инфекция или постинфекция) коррумпировало иммунную систему, а новая инфекция- случайно "поломала" имеющийся сбой в иммунитете, и сбросило настройки к первичным.
однако, и это в копилку того, что может быть одновременно несколько инфекционных процессов.
no subject
Date: 2025-02-11 04:05 am (UTC)Может быть, но скорее может не быть. Вот взять к примеру меня. За долгие 66 лет проживания я если и болел простудным вирусом, то каким-то чем-то одним. Если разными, то только по порядку и никогда вместе.
no subject
Date: 2025-02-11 04:31 am (UTC)однако, когда человек болеет ОРВИ, без специальных тестов не узнать, какой именно вирус или группа вирусов их вызвали. их более 300 известных, да еще и для каждого есть штаммы. а вот симптоматика у всех ОРВИ- похожая.