Containment and clearance of invading pathogens, such as viruses, by suppression of viral replication through antiviral mechanisms (e.g. CRISPR, interferon response or programmed cell death) provide examples of evolutionary developed responses by hosts to limit the establishment of infection. Degradation of the cytoplasm en masse provides an ideal cellular response against intruding pathogens. Degradation of such scale is achieved by a process called (macro)autophagy, where double membrane vacuoles, autophagosomes, engulf cytoplasm and organelles for lysosomal degradation. However, chronic and unrestrained autophagy poses catastrophic consequences to a cell especially when vital organelles (e.g. mitochondria or nucleus) are engulfed and destroyed. Recent findings in the field of autophagy and cell death regulation describe mechanisms that distinguish whether autophagy takes a moderate or excess route. This review aims to present new perspectives and re-examines current assumptions related to cell death regulation by autophagy. The emerging role of TAM receptors in the modulation of autophagy (i.e. both homeostatic and lethal) in the context of virus infections is also discussed in addition to chemical strategies for studying autophagy.

通过抗病毒机制（例如 CRISPR、干扰素反应或程序性细胞死亡）抑制病毒复制来遏制和清除入侵病原体，例如病毒，提供了宿主进化发展反应以限制感染建立的例子。胞浆降解集体为入侵的病原体提供理想的细胞反应。这种规模的降解是通过称为（宏观）自噬的过程实现的，其中双膜液泡、自噬体、吞噬细胞质和细胞器用于溶酶体降解。然而，慢性和不受限制的自噬会对细胞造成灾难性的后果，尤其是当重要的细胞器（例如线粒体或细胞核）被吞噬和破坏时。自噬和细胞死亡调节领域的最新发现描述了区分自噬是采取适度还是过度途径的机制。本综述旨在提出新的观点并重新审视当前与自噬调节细胞死亡相关的假设。TAM 受体在调节自噬（即