Browsing by Author "Farías León, Mónica Andrea"

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    Anti-herpetic Activity ofMacrocystis pyriferaandDurvillaea antarcticaAlgae Extracts Against HSV-1 and HSV-2
    (2020) Castillo, E.; Duarte Peñaloza, Luisa Fernanda; Corrales, N.; Álvarez Espejo, Diana Claudia Marcela; Farías León, Mónica Andrea; Henríquez, A.; Smith Ferrer, Patricio; Agurto Muñoz, C.; González Muñoz, Pablo Alberto
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    Experimental Dissection of the Lytic Replication Cycles of Herpes Simplex Viruses in vitro
    (2018) Ibáñez Irribarra, Francisco Javier; Farías León, Mónica Andrea; González Troncoso Mp; Corrales N.; Duarte Peñaloza, Luisa Fernanda; Retamal Díaz, Angello Ricardo; González Muñoz, Pablo Alberto
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    Heme Oxygenase-1 Expression in Dendritic Cells Contributes to Protective Immunity against Herpes Simplex Virus Skin Infection
    (MDPI, 2023) Tognarelli Torres, Eduardo Ignacio; Duarte Peñaloza, Luisa Fernanda; Farías León, Mónica Andrea; Cancino Prado, Felipe Andrés; Corrales Bonilla, Nicolas; Ibañez Irribarra, Francisco Javier; Riedel Soria, Claudia; Bueno Ramírez, Susan; Kalergis Parra,Alexis Mikes; González Muñoz, Pablo Alberto
    Herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) infections are highly prevalent in the human population and produce mild to life-threatening diseases. These viruses interfere with the function and viability of dendritic cells (DCs), which are professional antigen-presenting cells that initiate and regulate the host's antiviral immune responses. Heme oxygenase-1 (HO-1) is an inducible host enzyme with reported antiviral activity against HSVs in epithelial cells and neurons. Here, we sought to assess whether HO-1 modulates the function and viability of DCs upon infection with HSV-1 or HSV-2. We found that the stimulation of HO-1 expression in HSV-inoculated DCs significantly recovered the viability of these cells and hampered viral egress. Furthermore, HSV-infected DCs stimulated to express HO-1 promoted the expression of anti-inflammatory molecules, such as PDL-1 and IL-10, and the activation of virus-specific CD4(+) T cells with regulatory (Treg), Th17 and Treg/Th17 phenotypes. Moreover, HSV-infected DCs stimulated to express HO-1 and then transferred into mice, promoted the activation of virus-specific T cells and improved the outcome of HSV-1 skin infection. These findings suggest that stimulation of HO-1 expression in DCs limits the deleterious effects of HSVs over these cells and induces a favorable virus-specific immune response in the skin against HSV-1.
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    Herpes Simplex Virus Type 1 Infection of the Central Nervous System : Insights Into Proposed Interrelationships With Neurodegenerative Disorders
    (2019) Duarte Peñaloza, Luisa Fernanda; Farías León, Mónica Andrea; Álvarez Espejo, Diana Claudia Marcela; Bueno Ramírez, Susan; Riedel Soria, Claudia; González Muñoz, Pablo Alberto; Gonzalez-Dunia, Daniel
    Herpes simplex virus type 1 (HSV-1) is highly prevalent in humans and can reach the brain without evident clinical symptoms. Once in the central nervous system (CNS), the virus can either reside in a quiescent latent state in this tissue, or eventually actively lead to severe acute necrotizing encephalitis, which is characterized by exacerbated neuroinflammation and prolonged neuroimmune activation producing a life-threatening disease. Although HSV-1 encephalitis can be treated with antivirals that limit virus replication, neurological sequelae are common and the virus will nevertheless remain for life in the neural tissue. Importantly, there is accumulating evidence that suggests that HSV-1 infection of the brain both, in symptomatic and asymptomatic individuals could lead to neuronal damage and eventually, neurodegenerative disorders. Here, we review and discuss acute and chronic infection of particular brain regions by HSV-1 and how this may affect neuron and cognitive functions in the host. We review potential cellular and molecular mechanisms leading to neurodegeneration, such as protein aggregation, dysregulation of autophagy, oxidative cell damage and apoptosis, among others. Furthermore, we discuss the impact of HSV-1 infection on brain inflammation and its potential relationship with neurodegenerative diseases.
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    Study of lipid droplets role on the function of dendritic cells infected with herpes simplex virus type 1
    (2023) Farías León, Mónica Andrea; González Muñoz, Pablo Alberto; Pontificia Universidad Católica de Chile. Facultad de Ciencias Biológicas
    Herpes simplex virus type 1 (HSV-1) infection is highly prevalent in the human population and infections are lifelong, with sporadic reactivations that may elicit recurrent symptomatic disease. HSV-1 can evade the host immune response at multiple levels, by interfering with innate and adaptive immunity. Dendritic cells (DCs) are key immune cells that activate and regulate antiviral immune responses. DCs can activate CD4+ and CD8+ T cells, which can modulate the host antiviral immune response and elicit immunity. HSV- 1 infects DCs and alters their function by hampering their maturation, antigen-processing capacity, and migration to lymph nodes which alter their capacity to activate naïve T cells and mount an effective antiviral response. On the other hand, lipid droplets (LDs) are neutral lipid-rich organelles reported to negatively modulate DC function, decreasing the capacity of these cells to present antigens T cells and activate these cells. Here, we sought to assess whether HSV-1 alters lipid metabolism in DCs and induces LDs within these cells. Interestingly, we found that HSV-1 induces LDs in DCs, as well as significant changes in lipid metabolism processes, altering lipid accumulation and the expression of lipid metabolism-related genes. Importantly, we found that the pharmacological inhibition of lipid metabolism-related enzymes associated with fatty acid uptake and cholesterol ester synthesis inhibited LD accumulation in HSV-1-infected DCs, decreased virus yield. Furthermore, HSV-1-infected DCs treated with such drugs improved the viability of DCs and their capacity to activate virus-specific CD8+ T cells in vitro and migrate to lymph nodes to promote the activation of virus-specific CD8+ T cells in vivo. These findings indicate that HSV-1 infection significantly alters lipid metabolism in DCs, seemingly playing a significant role in the deterioration of the function of these cells upon infection with this virus.