The major innate immune cell types involved in tuberculosis(TB)infection are macrophages,dendritic cells(DCs),neutrophils and natural killer(NK)cells.These immune cells recognize the TB-causing pathogen Mycobacterium ...The major innate immune cell types involved in tuberculosis(TB)infection are macrophages,dendritic cells(DCs),neutrophils and natural killer(NK)cells.These immune cells recognize the TB-causing pathogen Mycobacterium tuberculosis(Mtb)through various pattern recognition receptors(PRRs),including but not limited to Toll-like receptors(TLRs),Nod-like receptors(NLRs)and C-type lectin receptors(CLRs).Upon infection by Mtb,the host orchestrates multiple signaling cascades via the PRRs to launch a variety of innate immune defense functions such as phagocytosis,autophagy,apoptosis and inflammasome activation.In contrast,Mtb utilizes numerous exquisite strategies to evade or circumvent host innate immunity.Here we discuss recent research on major host innate immune cells,PRR signaling,and the cellular functions involved in Mtb infection,with a specific focus on the host’s innate immune defense and Mtb immune evasion.A better understanding of the molecular mechanisms underlying host–pathogen interactions could provide a rational basis for the development of effective anti-TB therapeutics.展开更多
Drug resistance develops in nearly all patients with colon cancer, leading to a decrease in the therapeutic efficacies of anticancer agents. This review provides an up-to-date summary on over-expression of ATPbinding ...Drug resistance develops in nearly all patients with colon cancer, leading to a decrease in the therapeutic efficacies of anticancer agents. This review provides an up-to-date summary on over-expression of ATPbinding cassette(ABC) transporters and evasion of apoptosis, two representatives of transport-based and non-transport-based mechanisms of drug resistance, as well as their therapeutic strategies. Different ABC transporters were found to be up-regulated in colon cancer, which can facilitate the efflux of anticancer drugs out of cancer cells and decrease their therapeutic effects. Inhibition of ABC transporters by suppressing their protein expressions or co-administration of modulators has been proven as an effective approach to sensitize drug-resistant cancer cells to anticancer drugs in vitro. On the other hand, evasion of apoptosis observed in drug-resistant cancers also results in drug resistance to anticancer agents, especially to apoptosis inducers. Restoration of apoptotic signals by BH3 mimetics or epidermal growth factor receptor inhibitors and inhibition of cancer cell growth by alternative cell death pathways, such as autophagy, are effective means to treat such resistant cancer types. Given that the drug resistance mechanisms are different among colon cancer patients and may change even in a single patient at different stages, personalized and specific combination therapy is proposed to be more effective and safer for the reversal of drug resistance in clinics.展开更多
Hepatitis C imposes a significant burden on global healthcare. Chronic infection is associated with progressive inflammation of the liver which typically manifests in cirrhosis, organ failure and cancer. By virtue of ...Hepatitis C imposes a significant burden on global healthcare. Chronic infection is associated with progressive inflammation of the liver which typically manifests in cirrhosis, organ failure and cancer. By virtue of elaborate evasion strategies, hepatitis C virus （HCV） succeeds as a persistent human virus. It has an extraordinary capacity to subvert the immune response enabling it to establish chronic infections and associated liver disease. Chemokines are low molecular weight chemotactic peptides that mediate the recruitment of inflammatory cells into tissues and back into the lymphatics and peripheral blood. Thus, they are central to the temporal and spatial distribution of effector and regulatory immune cells. The interactions between chemokines and their cognate receptors help shape the immune response and therefore, have a major influence on the outcome of infection. However, chemokines represent a target for modulation by viruses including the HCV. HCV is known to modulate chemokine expression in vitro and may therefore enable its survival by subverting the immune response in vivo through altered leukocyte chemotaxis resulting in impaired viral clearance and the establishment of chronic low-grade inflammation. In this review, the roles of chemokines in acute and chronic HCV infection are described with a particular emphasis placed on chemokine modulation as a means of immune subversion. We provide an in depth discussion of the part played by chemokines in mediating hepatic fibrosis while addressing the potential applications for these chemoattractants in prognostic medicine.展开更多
The outcomes of hepatitis B virus(HBV) infection are closely related to the age at which infection was acquired. Infection acquired in adult life tends to be selflimited, in contrast to perinatal acquirement, for whic...The outcomes of hepatitis B virus(HBV) infection are closely related to the age at which infection was acquired. Infection acquired in adult life tends to be selflimited, in contrast to perinatal acquirement, for which chronic persistence of the HBV is a general outcome. Innate immunity plays an indispensable role in early virus infection, facilitating virus clearance. However, it has been reported that HBV is under-recognized and poorly eliminated by the innate immune system in the early stages of infection, possibly explaining the long-lasting persistence of viremia afterwards. Furthermore, due to the existence of covalently closed circular DNA, chronic HBV clearance is very difficult, even when patients are given interferon-α and nucleotide/nucleoside analogs for antiviral therapy. The mechanism by which HBV evades innate immune recognition and establishes persistent infection remains a subject of debate. Besides, some researchers are becoming more interested in how to eradicate chronic HBV infection by restoring or boosting innate immunity. This review aimed to summarize the current knowledge on how intrahepatocyte signaling pathways and innate immune cells act after the onset of HBV infection and how these actions are related to the persistence of HBV. We anticipate the insights presented herein to be helpful for future development of novel immune therapeutic strategies to fight HBV infection.展开更多
Epstein-Barr virus(EBV) is an oncogenic virus that ubiquitously establishes life-long persistence in humans. To ensure its survival and maintain its B cell transformation function, EBV has developed powerful strategie...Epstein-Barr virus(EBV) is an oncogenic virus that ubiquitously establishes life-long persistence in humans. To ensure its survival and maintain its B cell transformation function, EBV has developed powerful strategies to evade host immune responses. Emerging evidence has shown that micro RNAs(mi RNAs) are powerful regulators of the maintenance of cellular homeostasis. In this review, we summarize current progress on how EBV utilizes mi RNAs for immune evasion. EBV encodes mi RNAs targeting both viral and host genes involved in the immune response. The mi RNAs are found in two gene clusters, and recent studies have demonstrated that lack of these clusters increases the CD4^+ and CD8^+ T cell response of infected cells. These reports strongly indicate that EBV mi RNAs are critical for immune evasion. In addition, EBV is able to dysregulate the expression of a variety of host mi RNAs, which influence multiple immune-related molecules and signaling pathways. The transport via exosomes of EBV-regulated mi RNAs and viral proteins contributes to the construction and modification of the inflammatory tumor microenvironment.During EBV immune evasion, viral proteins, immune cells, chemokines, pro-inflammatory cytokines, and pro-apoptosis molecules are involved. Our increasing knowledge of the role of mi RNAs in immune evasion will improve the understanding of EBV persistence and help to develop new treatments for EBV-associated cancers and other diseases.展开更多
This paper presents a novel evasion guidance law for hypersonic morphing vehicles,focusing on determining the optimized wing's unfolded angle to promote maneuverability based on an intelligent algorithm.First,the ...This paper presents a novel evasion guidance law for hypersonic morphing vehicles,focusing on determining the optimized wing's unfolded angle to promote maneuverability based on an intelligent algorithm.First,the pursuit-evasion problem is modeled as a Markov decision process.And the agent's action consists of maneuver overload and the unfolded angle of wings,which is different from the conventional evasion guidance designed for fixed-shape vehicles.The reward function is formulated to ensure that the miss distances satisfy the prescribed bounds while minimizing energy consumption.Then,to maximize the expected cumulative reward,a residual learning method is proposed based on proximal policy optimization,which integrates the optimal evasion for linear cases as the baseline and trains to optimize the performance for nonlinear engagement with multiple pursuers.Therefore,offline training guarantees improvement of the constructed evasion guidance law over conventional ones.Ultimately,the guidance law for online implementation includes only analytical calculations.It maps from the confrontation state to the expected angle of attack and the unfolded angle while retaining high computational efficiency.Simulations show that the proposed evasion guidance law can utilize the change of unfolded angle to extend the maximum overload capability.And it surpasses conventional maneuver strategies by ensuring better evasion efficacy and higher energy efficiency.展开更多
While the host immune response following primary human cytomegalovirus （HCMV） infection is generally effective at stopping virus replication and dissemination, virus is never cleared by the host and like all herpesv...While the host immune response following primary human cytomegalovirus （HCMV） infection is generally effective at stopping virus replication and dissemination, virus is never cleared by the host and like all herpesviruses, persists for life. At least in part, this persistence is known to be facilitated by the ability of HCMV to establish latency in myeloid cells in which infection is essentially silent with, importantly, a total lack of new virus production. However, although the viral transcription programme during latency is much suppressed, a number of viral genes are expressed during latent infection at the protein level and many of these have been shown to have profound effects on the latent cell and its environment. Intriguingly, many of these latency-associated genes are also expressed during lyric infection. Therefore, why the same potent host immune responses generated during lytic infection to these viral gene products are not recognized during latency, thereby allowing clearance of latently infected cells, is far from clear. Reactivation from latency is also a major cause of HCMV-mediated disease, particularly in the immune compromised and immune naive, and is also likely to be a major source of virus in chronic subclinical HCMV infection which has been suggested to be associated with long-term diseases such as atherosclerosis and some neoplasias. Consequently, understanding latency and why latenUy infected cells appear to be immunoprivileged is crucial for an understanding of the pathogenesis of HCMV and may help to design strategies to eliminate latent virus reservoirs, at least in certain clinical settings.展开更多
Hepatitis B virus(HBV) infection is still a worldwide health problem;however,the current antiviral therapies for chronic hepatitis B are limited in efficacy.The outcome of HBV infection is thought to be the result of ...Hepatitis B virus(HBV) infection is still a worldwide health problem;however,the current antiviral therapies for chronic hepatitis B are limited in efficacy.The outcome of HBV infection is thought to be the result of complex interactions between the HBV and the host immune system.While the role of the adaptive immune responses in the resolution of HBV infection has been well characterized,the contribution of innate immune mechanisms remains elusive until recent evidence implicates that HBV appears to activate the innate immune response and this response is important for controlling HBV infection.Here,we review our current understanding of innate immune responses to HBV infection and the multifaceted evasion by the virus and discuss the potential strategies to combat chronic HBV infection via induction and restoration of host innate antiviral responses.展开更多
Small ubiquitin-like modifier(SUMO)ylation is a key posttranslational modification mechanism that controls the function of a plethora of proteins and biological processes. Given its central regulatory role, it is not ...Small ubiquitin-like modifier(SUMO)ylation is a key posttranslational modification mechanism that controls the function of a plethora of proteins and biological processes. Given its central regulatory role, it is not surprising that it is widely exploited by viruses. A number of viral proteins are known to modify and/or be modified by the SUMOylation system to exert their function, to create a cellular environment more favorable for virus survival and propagation, and to prevent host antiviral responses. Since the SUMO pathway is a multi-step cascade, viral proteins engage with it at many levels, to advance and favor each stage of a typical infection cycle: replication, viral assembly and immune evasion. Here we review the current knowledge on the interplay between the host SUMO system and viral lifecycle.展开更多
This paper investigates a new approach for a scenario in which an Attacker attempts to intercept a defended aerial Target. The problem is formulated as a game among three players, an Attacker, a Defender, and a Target...This paper investigates a new approach for a scenario in which an Attacker attempts to intercept a defended aerial Target. The problem is formulated as a game among three players, an Attacker, a Defender, and a Target, with bounded controls. In the considered pursuit–evasion problem, the Target uses an optimal evasion strategy and the Defender uses an optimal pursuit strategy.The proposed approach focuses on the miss distance as the outcome of the conflict. The infeasible region for the initial Zero-Effort-Miss（ZEM） distance between the Attacker and the Defender, for a scenario in which the Attacker evades the Defender, is analyzed, assuming that the Attacker uses a control effort chosen from the permitted control region. The sufficient conditions are investigated under which, for ideal players, the Attacker can pursue the Target while evading the Defender launched by the Target. The guidance provided on how the Attacker can accomplish the task is divided into two parts. During the final time between the Attacker and the Defender, the Attacker chooses the control effort that guarantees the miss distance, and then uses the optimal pursuit strategy to accomplish the task. The derived guidance law is verified by nonlinear simulation.展开更多
Cellular sensing of virus-derived nucleic acids is essential for early defenses against virus infections. In recent years, the discovery of DNA sensing proteins, including cyclic GMP-AMP synthase （cGAS） and gamma-in...Cellular sensing of virus-derived nucleic acids is essential for early defenses against virus infections. In recent years, the discovery of DNA sensing proteins, including cyclic GMP-AMP synthase （cGAS） and gamma-interferon- inducible protein （IFI16）, has led to understanding of how cells evoke strong innate immune responses against incoming pathogens carrying DNA genomes. The signaling stimulated by DNA sensors depends on the adaptor protein STING （stimulator of interferon genes）, to enable expression of antiviral proteins, including type I interferon. To facilitate efficient infections, viruses have evolved a wide range of evasion strategies, targeting host DNA sensors, adaptor proteins and transcription factors. In this review, the current literature on virus-induced activation of the STING pathway is presented and we discuss recently identified viral evasion mechanisms targeting different steps in this antiviral pathway.展开更多
基金the National Key Research and Development Program of China(Grant Nos.2017YFA0505900 and 2017YFD0500300)the National Basic Research Programs of China(Grant No.2014CB74440)+2 种基金the National Natural Science Foundation of China(Grant Nos.81371769 and 81571954)the Strategic Priority Research Program of the Chinese Academy of Sciences(Grant No.XDPB03)the Youth Innovation Promotion Association CAS(Grant No.Y12A027BB2).
文摘The major innate immune cell types involved in tuberculosis(TB)infection are macrophages,dendritic cells(DCs),neutrophils and natural killer(NK)cells.These immune cells recognize the TB-causing pathogen Mycobacterium tuberculosis(Mtb)through various pattern recognition receptors(PRRs),including but not limited to Toll-like receptors(TLRs),Nod-like receptors(NLRs)and C-type lectin receptors(CLRs).Upon infection by Mtb,the host orchestrates multiple signaling cascades via the PRRs to launch a variety of innate immune defense functions such as phagocytosis,autophagy,apoptosis and inflammasome activation.In contrast,Mtb utilizes numerous exquisite strategies to evade or circumvent host innate immunity.Here we discuss recent research on major host innate immune cells,PRR signaling,and the cellular functions involved in Mtb infection,with a specific focus on the host’s innate immune defense and Mtb immune evasion.A better understanding of the molecular mechanisms underlying host–pathogen interactions could provide a rational basis for the development of effective anti-TB therapeutics.
文摘Drug resistance develops in nearly all patients with colon cancer, leading to a decrease in the therapeutic efficacies of anticancer agents. This review provides an up-to-date summary on over-expression of ATPbinding cassette(ABC) transporters and evasion of apoptosis, two representatives of transport-based and non-transport-based mechanisms of drug resistance, as well as their therapeutic strategies. Different ABC transporters were found to be up-regulated in colon cancer, which can facilitate the efflux of anticancer drugs out of cancer cells and decrease their therapeutic effects. Inhibition of ABC transporters by suppressing their protein expressions or co-administration of modulators has been proven as an effective approach to sensitize drug-resistant cancer cells to anticancer drugs in vitro. On the other hand, evasion of apoptosis observed in drug-resistant cancers also results in drug resistance to anticancer agents, especially to apoptosis inducers. Restoration of apoptotic signals by BH3 mimetics or epidermal growth factor receptor inhibitors and inhibition of cancer cell growth by alternative cell death pathways, such as autophagy, are effective means to treat such resistant cancer types. Given that the drug resistance mechanisms are different among colon cancer patients and may change even in a single patient at different stages, personalized and specific combination therapy is proposed to be more effective and safer for the reversal of drug resistance in clinics.
文摘Hepatitis C imposes a significant burden on global healthcare. Chronic infection is associated with progressive inflammation of the liver which typically manifests in cirrhosis, organ failure and cancer. By virtue of elaborate evasion strategies, hepatitis C virus （HCV） succeeds as a persistent human virus. It has an extraordinary capacity to subvert the immune response enabling it to establish chronic infections and associated liver disease. Chemokines are low molecular weight chemotactic peptides that mediate the recruitment of inflammatory cells into tissues and back into the lymphatics and peripheral blood. Thus, they are central to the temporal and spatial distribution of effector and regulatory immune cells. The interactions between chemokines and their cognate receptors help shape the immune response and therefore, have a major influence on the outcome of infection. However, chemokines represent a target for modulation by viruses including the HCV. HCV is known to modulate chemokine expression in vitro and may therefore enable its survival by subverting the immune response in vivo through altered leukocyte chemotaxis resulting in impaired viral clearance and the establishment of chronic low-grade inflammation. In this review, the roles of chemokines in acute and chronic HCV infection are described with a particular emphasis placed on chemokine modulation as a means of immune subversion. We provide an in depth discussion of the part played by chemokines in mediating hepatic fibrosis while addressing the potential applications for these chemoattractants in prognostic medicine.
基金supported by Natural Science Foundation of China,No.81500455
文摘The outcomes of hepatitis B virus(HBV) infection are closely related to the age at which infection was acquired. Infection acquired in adult life tends to be selflimited, in contrast to perinatal acquirement, for which chronic persistence of the HBV is a general outcome. Innate immunity plays an indispensable role in early virus infection, facilitating virus clearance. However, it has been reported that HBV is under-recognized and poorly eliminated by the innate immune system in the early stages of infection, possibly explaining the long-lasting persistence of viremia afterwards. Furthermore, due to the existence of covalently closed circular DNA, chronic HBV clearance is very difficult, even when patients are given interferon-α and nucleotide/nucleoside analogs for antiviral therapy. The mechanism by which HBV evades innate immune recognition and establishes persistent infection remains a subject of debate. Besides, some researchers are becoming more interested in how to eradicate chronic HBV infection by restoring or boosting innate immunity. This review aimed to summarize the current knowledge on how intrahepatocyte signaling pathways and innate immune cells act after the onset of HBV infection and how these actions are related to the persistence of HBV. We anticipate the insights presented herein to be helpful for future development of novel immune therapeutic strategies to fight HBV infection.
基金supported by the National Natural Science Foundations of China(81372139,31670171)the Hunan Provincial Natural Science Foundation of China(2015JJ2149)the Hunan Provincial Innovation Foundation for Postgraduates(CX2016B055)
文摘Epstein-Barr virus(EBV) is an oncogenic virus that ubiquitously establishes life-long persistence in humans. To ensure its survival and maintain its B cell transformation function, EBV has developed powerful strategies to evade host immune responses. Emerging evidence has shown that micro RNAs(mi RNAs) are powerful regulators of the maintenance of cellular homeostasis. In this review, we summarize current progress on how EBV utilizes mi RNAs for immune evasion. EBV encodes mi RNAs targeting both viral and host genes involved in the immune response. The mi RNAs are found in two gene clusters, and recent studies have demonstrated that lack of these clusters increases the CD4^+ and CD8^+ T cell response of infected cells. These reports strongly indicate that EBV mi RNAs are critical for immune evasion. In addition, EBV is able to dysregulate the expression of a variety of host mi RNAs, which influence multiple immune-related molecules and signaling pathways. The transport via exosomes of EBV-regulated mi RNAs and viral proteins contributes to the construction and modification of the inflammatory tumor microenvironment.During EBV immune evasion, viral proteins, immune cells, chemokines, pro-inflammatory cytokines, and pro-apoptosis molecules are involved. Our increasing knowledge of the role of mi RNAs in immune evasion will improve the understanding of EBV persistence and help to develop new treatments for EBV-associated cancers and other diseases.
基金This work was supported by the National Natural Science Foundation of China(No.52202438).
文摘This paper presents a novel evasion guidance law for hypersonic morphing vehicles,focusing on determining the optimized wing's unfolded angle to promote maneuverability based on an intelligent algorithm.First,the pursuit-evasion problem is modeled as a Markov decision process.And the agent's action consists of maneuver overload and the unfolded angle of wings,which is different from the conventional evasion guidance designed for fixed-shape vehicles.The reward function is formulated to ensure that the miss distances satisfy the prescribed bounds while minimizing energy consumption.Then,to maximize the expected cumulative reward,a residual learning method is proposed based on proximal policy optimization,which integrates the optimal evasion for linear cases as the baseline and trains to optimize the performance for nonlinear engagement with multiple pursuers.Therefore,offline training guarantees improvement of the constructed evasion guidance law over conventional ones.Ultimately,the guidance law for online implementation includes only analytical calculations.It maps from the confrontation state to the expected angle of attack and the unfolded angle while retaining high computational efficiency.Simulations show that the proposed evasion guidance law can utilize the change of unfolded angle to extend the maximum overload capability.And it surpasses conventional maneuver strategies by ensuring better evasion efficacy and higher energy efficiency.
文摘While the host immune response following primary human cytomegalovirus （HCMV） infection is generally effective at stopping virus replication and dissemination, virus is never cleared by the host and like all herpesviruses, persists for life. At least in part, this persistence is known to be facilitated by the ability of HCMV to establish latency in myeloid cells in which infection is essentially silent with, importantly, a total lack of new virus production. However, although the viral transcription programme during latency is much suppressed, a number of viral genes are expressed during latent infection at the protein level and many of these have been shown to have profound effects on the latent cell and its environment. Intriguingly, many of these latency-associated genes are also expressed during lyric infection. Therefore, why the same potent host immune responses generated during lytic infection to these viral gene products are not recognized during latency, thereby allowing clearance of latently infected cells, is far from clear. Reactivation from latency is also a major cause of HCMV-mediated disease, particularly in the immune compromised and immune naive, and is also likely to be a major source of virus in chronic subclinical HCMV infection which has been suggested to be associated with long-term diseases such as atherosclerosis and some neoplasias. Consequently, understanding latency and why latenUy infected cells appear to be immunoprivileged is crucial for an understanding of the pathogenesis of HCMV and may help to design strategies to eliminate latent virus reservoirs, at least in certain clinical settings.
基金supported by the German ResearchFoundation(SFB/Transregio TRR60)the InternationalScience&Technology Cooperation Program of China(Grant 2011DFA31030)the National Key BasicResearch Program of China(2012CB519005)
文摘Hepatitis B virus(HBV) infection is still a worldwide health problem;however,the current antiviral therapies for chronic hepatitis B are limited in efficacy.The outcome of HBV infection is thought to be the result of complex interactions between the HBV and the host immune system.While the role of the adaptive immune responses in the resolution of HBV infection has been well characterized,the contribution of innate immune mechanisms remains elusive until recent evidence implicates that HBV appears to activate the innate immune response and this response is important for controlling HBV infection.Here,we review our current understanding of innate immune responses to HBV infection and the multifaceted evasion by the virus and discuss the potential strategies to combat chronic HBV infection via induction and restoration of host innate antiviral responses.
文摘Small ubiquitin-like modifier(SUMO)ylation is a key posttranslational modification mechanism that controls the function of a plethora of proteins and biological processes. Given its central regulatory role, it is not surprising that it is widely exploited by viruses. A number of viral proteins are known to modify and/or be modified by the SUMOylation system to exert their function, to create a cellular environment more favorable for virus survival and propagation, and to prevent host antiviral responses. Since the SUMO pathway is a multi-step cascade, viral proteins engage with it at many levels, to advance and favor each stage of a typical infection cycle: replication, viral assembly and immune evasion. Here we review the current knowledge on the interplay between the host SUMO system and viral lifecycle.
基金supported by the National Natural Science Foundation of China (No. 11672093)Shanghai Aerospace Science and Technology Innovation Foundation of China (No. SAST2016039)
文摘This paper investigates a new approach for a scenario in which an Attacker attempts to intercept a defended aerial Target. The problem is formulated as a game among three players, an Attacker, a Defender, and a Target, with bounded controls. In the considered pursuit–evasion problem, the Target uses an optimal evasion strategy and the Defender uses an optimal pursuit strategy.The proposed approach focuses on the miss distance as the outcome of the conflict. The infeasible region for the initial Zero-Effort-Miss（ZEM） distance between the Attacker and the Defender, for a scenario in which the Attacker evades the Defender, is analyzed, assuming that the Attacker uses a control effort chosen from the permitted control region. The sufficient conditions are investigated under which, for ideal players, the Attacker can pursue the Target while evading the Defender launched by the Target. The guidance provided on how the Attacker can accomplish the task is divided into two parts. During the final time between the Attacker and the Defender, the Attacker chooses the control effort that guarantees the miss distance, and then uses the optimal pursuit strategy to accomplish the task. The derived guidance law is verified by nonlinear simulation.
文摘Cellular sensing of virus-derived nucleic acids is essential for early defenses against virus infections. In recent years, the discovery of DNA sensing proteins, including cyclic GMP-AMP synthase （cGAS） and gamma-interferon- inducible protein （IFI16）, has led to understanding of how cells evoke strong innate immune responses against incoming pathogens carrying DNA genomes. The signaling stimulated by DNA sensors depends on the adaptor protein STING （stimulator of interferon genes）, to enable expression of antiviral proteins, including type I interferon. To facilitate efficient infections, viruses have evolved a wide range of evasion strategies, targeting host DNA sensors, adaptor proteins and transcription factors. In this review, the current literature on virus-induced activation of the STING pathway is presented and we discuss recently identified viral evasion mechanisms targeting different steps in this antiviral pathway.
