Producción de Penicilina en Chile entre 1944 y 1954

Ibarra, Cecilia; Parada, Mirtha

doi:10.4067/s0716-10182015000200013

Cited by 10 publications

(9 citation statements)

References 11 publications

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“…DCs degrade protein-derived antigens and present them to T cells as small peptides loaded on MHC-I and -II molecules (pMHC) that can be recognized by T cell receptors (TCR) on the surface of CD8 + and CD4 + T cells, respectively (Galvez et al, 2016). DC antigen presentation to T cells can lead to a process termed the immunological synapse, which involves close DC-T cell interactions that can result either in T cell activation or its inactivation (Gonzalez et al, 2007; Murphy et al, 2012; Retamal-Diaz et al, 2015; Retamal-Diaz A. et al, 2017). Importantly, the interaction between DCs and antigen-specific T cells will determine the phenotype of T cells which will depend on the expression of membrane-bound and soluble molecules presented at the cell-cell interphase (Zheng et al, 2004).…”

Section: Hsv Infection Modulates Dendritic Cell Maturation Antiviralmentioning

confidence: 99%

“…Importantly, HSVs not only infect epithelial cells and neurons but virtually any cell type in the body, including immune cells thanks to the fact that the main receptors of HSVs are widely distributed in host tissues and cells (Krummenacher et al, 2004). By infecting immune cells, these viruses can modulate and escape diverse antiviral mechanisms evolved by the host to counteract infection and furthermore, establish long-term infection with sporadic recurrences that produce new infectious particles (Retamal-Diaz et al, 2015; Suazo et al, 2015a). Here, we review and discuss recent studies that report the relationship between HSVs and early cellular antiviral responses, both in immune and non-immune cells.…”

Section: Introductionmentioning

confidence: 99%

“…The viral genomes are covered by a 125 nm icosahedral capsid (Wu et al, 2016), which is surrounded by a mesh composed by many proteins (>20) called the tegument (Figure 1). This protein stratum is in turn enveloped by a lipid bilayer, from which multiple viral glycoproteins protrude and play roles in virus entry and exit, as well as immune-modulation and immune-escape (Roller and Roizman, 1992; Loret et al, 2008; Retamal-Diaz et al, 2015; Suazo et al, 2015a; Suk and Knipe, 2015).…”

Section: Introductionmentioning

confidence: 99%

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Herpes Simplex Virus Evasion of Early Host Antiviral Responses

Tognarelli

Palomino

Corrales

et al. 2019

Front. Cell. Infect. Microbiol.

100

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Herpes simplex viruses type 1 (HSV-1) and type 2 (HSV-2) have co-evolved with humans for thousands of years and are present at a high prevalence in the population worldwide. HSV infections are responsible for several illnesses including skin and mucosal lesions, blindness and even life-threatening encephalitis in both, immunocompetent and immunocompromised individuals of all ages. Therefore, diseases caused by HSVs represent significant public health burdens. Similar to other herpesviruses, HSV-1 and HSV-2 produce lifelong infections in the host by establishing latency in neurons and sporadically reactivating from these cells, eliciting recurrences that are accompanied by viral shedding in both, symptomatic and asymptomatic individuals. The ability of HSVs to persist and recur in otherwise healthy individuals is likely given by the numerous virulence factors that these viruses have evolved to evade host antiviral responses. Here, we review and discuss molecular mechanisms used by HSVs to evade early innate antiviral responses, which are the first lines of defense against these viruses. A comprehensive understanding of how HSVs evade host early antiviral responses could contribute to the development of novel therapies and vaccines to counteract these viruses.

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Section: Hsv Infection Modulates Dendritic Cell Maturation Antiviralmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Herpes Simplex Virus Evasion of Early Host Antiviral Responses

Tognarelli

Palomino

Corrales

et al. 2019

Front. Cell. Infect. Microbiol.

100

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“…Furthermore, this viral protein harbors epitopes for CD4 + T cells [222], CD8 + T cells [223], and neutralizing antibodies [224] and is immunodominant as evidenced by clinical data showing that the majority of HSVinfected individuals have neutralizing antibodies against this protein [199]. Regretfully, this insisted strategy, which combines gD with adjuvants, recently failed in a phase 3 clinical trial; indeed, the formulation failed at reducing both HSV-2 infection and minimizing the shedding of the virus [225,226]. Remarkably, the formulation tested in this and previous clinical trials induced anti-gD neutralizing antibodies in the vaccinated, as well as T CD4 + cells [220,[227][228][229][230].…”

Section: Past and Present Vaccine Attemptsmentioning

confidence: 99%

Immune Evasion by Herpes Simplex Viruses

Retamal-Díaz¹,

Tognarelli²,

Kalergis³

et al. 2016

Herpesviridae

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Infection with herpes simplex viruses type HSV-and type HSV-is extremely frequent in the human population, as well as recurrent reactivations due to lifelong infection. Infection and persistence of HSVs within healthy individuals likely results as a consequence of numerous molecular determinants evolved by these pathogens to escape both immediate and long-term host antiviral mechanisms. Indeed, HSVs harbor an arsenal of proteins that confer them stealth by negatively modulating immune function. Consequently, these viruses perpetuate within the host, altogether silently shedding onto other individuals. In this chapter, we discuss HSV determinants that interfere with cellular antiviral factors, as well as viral determinants that hamper innate and adaptive immune components intended to control such microbes. The identification of HSV evasion molecules that modulate the immune system, as well as the understanding of their mechanisms of action, should facilitate the design of novel prophylactic and therapeutic strategies to overcome infection and disease elicited by these viruses. This chapter is intended to provide an overview of the evasion mechanisms evolved by herpes simplex viruses to escape numerous host antiviral mediators.

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“…Important efforts have been invested in the past 20 years on the development of a vaccine against HSVs. However, potential vaccine formulations that have reached the clinic have proven ineffective at preventing infection or reducing virus shedding [ 35 , 36 ]. Discouraging results derived from the latest HSV-2 vaccine clinical trial, which used a viral subunit formulation, have led to new debates in the field and rethinking on the role of neutralizing antibodies in protecting against HSV-2, as well as the need for correlates of protection [ 37 – 39 ].…”

Section: Introductionmentioning

confidence: 99%

Evasion of Early Antiviral Responses by Herpes Simplex Viruses

Suazo

Ibáñez

Retamal-Díaz

et al. 2015

Mediators of Inflammation

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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.

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Producción de Penicilina en Chile entre 1944 y 1954

Cited by 10 publications

References 11 publications

Herpes Simplex Virus Evasion of Early Host Antiviral Responses

Herpes Simplex Virus Evasion of Early Host Antiviral Responses

Immune Evasion by Herpes Simplex Viruses

Evasion of Early Antiviral Responses by Herpes Simplex Viruses

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