Background In order to understand the intricate patterns of interplay connected to the formation and maintenance of depressive symptomatology, repeated measures investigations focusing on within-person relationships between psychopathological mechanisms and depressive components are required. Methods This large-scale preregistered intensive longitudinal study conducted 68,240 observations of 1706 individuals in the general adult population across a 40-day period during the COVID-19 pandemic to identify the detrimental processes involved in depressive states. Daily responses were modeled using multi-level dynamic network analysis to investigate the temporal associations across days, in addition to contemporaneous relationships between depressive components within a daily window. Results Among the investigated psychopathological mechanisms, helplessness predicted the strongest across-day influence on depressive symptoms, while emotion regulation difficulties displayed more proximal interactions with symptomatology. Helplessness was further involved in the amplification of other theorized psychopathological mechanisms including rumination, the latter of which to a greater extent was susceptible toward being influenced rather than temporally influencing other components of depressive states. Distinctive symptoms of depression behaved differently, with depressed mood and anhedonia most prone to being impacted, while lethargy and worthlessness were more strongly associated with outgoing activity in the network. Conclusions The main mechanism predicting the amplifications of detrimental symptomatology was helplessness. Lethargy and worthlessness revealed greater within-person carry-over effects across days, providing preliminary indications that these symptoms may be more strongly associated with pushing individuals toward prolonged depressive state experiences. The psychopathological processes of rumination, helplessness, and emotion regulation only exhibited interactions with the depressed mood and worthlessness component of depression, being unrelated to lethargy and anhedonia. The findings have implications for the impediment of depressive symptomatology during and beyond the pandemic period. They further outline the gaps in the literature concerning the identification of psychopathological processes intertwined with lethargy and anhedonia on the within-person level.