Evasion of early antiviral responses by herpes simplex viruses.
Besides overcoming physical constraints, such as extreme temperatures, reduced humidity, elevated pressure, and natural predators, human pathogens further need to overcome an arsenal of antimicrobial components evolved by the host to limit infection, replication and optimally, reinfection. Herpes simplex virus-1 (HSV-1) and herpes simplex virus-2 (HSV-2) infect humans at a high frequency and persist within the host for life by establishing latency in neurons. To gain access to these cells, herpes simplex viruses (HSVs) must replicate and block immediate host antiviral responses elicited by epithelial cells and innate immune components early after infection. During these processes, infected and noninfected neighboring cells, as well as tissue-resident and patrolling immune cells, will sense viral components and cell-associated danger signals and secrete soluble mediators. While type-I interferons aim at limiting virus spread, cytokines and chemokines will modulate resident and incoming immune cells. In this paper, we discuss recent findings relative to the early steps taking place during HSV infection and replication. Further, we discuss how HSVs evade detection by host cells and the molecular mechanisms evolved by these viruses to circumvent early antiviral mechanisms, ultimately leading to neuron infection and the establishment of latency.
Millennium Institute on Immunology and Immunotherapy, Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, 8331010 Santiago, Chile.
Paula A
PA
Suazo
Millennium Institute on Immunology and Immunotherapy, Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, 8331010 Santiago, Chile.
Francisco J
FJ
Ibañez
Millennium Institute on Immunology and Immunotherapy, Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, 8331010 Santiago, Chile.
Angello R
AR
Retamal-Díaz
Millennium Institute on Immunology and Immunotherapy, Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, 8331010 Santiago, Chile.
Marysol V
MV
Paz-Fiblas
Millennium Institute on Immunology and Immunotherapy, Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, 8331010 Santiago, Chile ; INSERM UMR1064, 44093 Nantes, France.
Susan M
SM
Bueno
Millennium Institute on Immunology and Immunotherapy, Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, 8331010 Santiago, Chile ; INSERM UMR1064, 44093 Nantes, France ; Departamento de Inmunología Clínica y Reumatología, Escuela de Medicina, Facultad de Medicina, Pontificia Universidad Católica de Chile, 8331010 Santiago, Chile.
Alexis M
AM
Kalergis
Millennium Institute on Immunology and Immunotherapy, Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, 8331010 Santiago, Chile.
Pablo A
PA
González
D000818:Animals; D000998:Antiviral Agents / Q000737:chemistry*; D017209:Apoptosis; D002470:Cell Survival; D018925:Chemokines / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D004847:Epithelial Cells / Q000821:virology; D006561:Herpes Simplex / Q000276:immunology / Q000821:virology*; D018259:Herpesvirus 1, Human / Q000378:metabolism*; D006801:Humans; D007113:Immunity, Innate; D007372:Interferons / Q000378:metabolism; D009474:Neurons / Q000378:metabolism / Q000821:virology; D015398:Signal Transduction; D014779:Virus Replication
D000998:Antiviral Agents; D018925:Chemokines; D016207:Cytokines; D007372:Interferons