Management of acute viral encephalitis in Brazil

Domingues, Renan Barros; Teixeira, Antônio Lúcio

doi:10.1590/s1413-86702009000600009

Cited by 16 publications

(16 citation statements)

References 72 publications

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“…Herpes Simplex Virus (HSV) is a major cause of encephalitis in humans [1]. Conventional treatment of HSV-1 encephalitis (HSE) involves the use of antiviral therapies, current guidelines for the treatment of HSV-1 recommend intravenous acyclovir [2].…”

Section: Introductionmentioning

confidence: 99%

Absence of CCR5 increases neutrophil recruitment in severe herpetic encephalitis

Vilela

Lima

Rodrigues³

et al. 2013

BMC Neurosci

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BackgroundThe neuroinflammatory response aimed at clearance of herpes simplex virus-1 (HSV-1) plays a key role in the pathogenesis of neuroaxonal damage in herpetic encephalitis. Leukocytes activated in an adaptive immune response access brain tissue by passing through the blood–brain barrier. The chemokine CCL5/RANTES is involved in recruitment of these cells to the brain acting via the receptors CCR1, CCR3 and mainly CCR5. Here, we evaluated the role of CCR5 on traffic of leukocytes in the brain microvasculature, cellular and cytokines profile in a severe form of herpetic encephalitis.ResultsWild type and mice lacking CCR5 (CCR5-/-) were inoculated intracerebrally with 104 PFU of neurotropic HSV-1. We evaluated the traffic of leukocytes in the brain microvasculature using intravital microscopy and the profile of cytokines by Enzyme-Linked Immunosorbent Assay at 1 day post infection. Flow cytometry and histopathological analyses were also carried out in brain tissue. Absence of CCR5 leads to lower viral load and an increased leukocyte adhesion in brain microvasculature, predominantly of neutrophils (CD11+ Ly6G+ cells). Moreover, there was a significant increase in the levels of MIP-1/CCL2, RANTES/CCL5, KC/CXCL1 and MIG/CXCL9 in the brain of infected CCR5-/- mice.ConclusionsThese results suggest that the absence of CCR5 may boost the immune response with a high neutrophil recruitment which most likely helps in viral clearance. Nonetheless, the elevated immune response may be detrimental to the host.

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Section: Introductionmentioning

confidence: 99%

Absence of CCR5 increases neutrophil recruitment in severe herpetic encephalitis

Vilela

Lima

Rodrigues³

et al. 2013

BMC Neurosci

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“…Encephalitis caused by HSV-1 has a mortality rate of up to 20% and neurological sequelae in over 50% of survivors (Raschilas et al 2002;Domingues and Teixeira 2009). Standard treatment relies on the use of antiviral drugs and clinical support.…”

Section: Discussionmentioning

confidence: 99%

“…The activation of HSV-1 may result in Herpes Simplex Encephalitis (HSE), the main cause of sporadic acute focal encephalitis in humans (Whitley and Roizman 2001;Domingues and Teixeira 2009). Untreated HSV-1 encephalitis has a 70 % mortality rate and patients who receive early treatment have only a 40 % chance of recovery without significant neurological deficits (Baringer 2008).…”

Section: Introductionmentioning

confidence: 99%

Platelet Activating Factor (PAF) Receptor Deletion or Antagonism Attenuates Severe HSV-1 Meningoencephalitis

Vilela

Lima

Rodrigues

et al. 2016

J Neuroimmune Pharmacol

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Herpes simplex virus type 1 (HSV-1) is a human pathogen that may cause severe encephalitis. The exacerbated immune response against the virus contributes to the disease severity and death. Platelet activating factor (PAF) is a mediator capable of inducing increase in vascular permeability, production of cytokines on endothelial cells and leukocytes. We aimed to investigate the activation of PAF receptor (PAFR) and its contribution to the severity of the inflammatory response in the brain following HSV-1 infection. C57BL/6 wild-type (WT) and PAFR deficient (PAFR) mice were inoculated intracranially with 10 plaque-forming units (PFU) of HSV-1. Visualization of leukocyte recruitment was performed using intravital microscopy. Cells infiltration in the brain tissue were analyzed by flow cytometry. Brain was removed for chemokine assessment by ELISA and for histopathological analysis. The pharmacological inhibition by the PAFR antagonist UK-74,505 was also analyzed. In PAFR mice, there was delayed lethality but no difference in viral load. Histopathological analysis of infected PAFR mice showed that brain lesions were less severe when compared to their WT counterparts. Moreover, PAFR mice showed less TCD4, TCD8 and macrophages in brain tissue. This reduction of the presence of leukocytes in parenchyma may be mechanistically explained by a decrease in leukocytes rolling and adhesion. PAFR mice also presented a reduction of the chemokine CXCL9 in the brain. In addition, by antagonizing PAFR, survival of C57BL/6 infected mice increased. Altogether, our data suggest that PAFR plays a role in the pathogenesis of experimental HSV-1 meningoencephalitis, and its blockade prevents severe disease manifestation.

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“…In cases of HSE, acyclovir must be introduced early because its efficacy is greater during the earlier stages of infection [7,21,119]. Fatal outcomes and severe neurological sequelae are frequently observed.…”

Section: Discussionmentioning

confidence: 99%

Viral Encephalitis: Current Treatments and Future Perspectives

Domingues

2012

CNSAMC

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Several viruses may cause central nervous system infections that lead to a broad range of clinical manifestations. The course of the viral encephalitis can be acute, sub acute, or chronic. Some viruses have the ability to enter into the brain and cause direct injury, while others activate inflammatory cells that attack the central nervous system (CNS) secondarily. Some types of viral encephalitis occur in previously healthy individuals, while others affect immunocompromised patients. The epidemiology of viral encephalitis has undergone changes in recent years. Factors such as evolving lifestyles and ecological changes have had a considerable impact on the epidemiology of some types of viral encephalitis. The result is a change in the etiology spectrum of viral encephalitis, with new types of encephalitis arising or returning from time to time. Many scientific achievements in neuroimaging, molecular diagnosis, antiviral therapy, immunomodulatory treatments, and neurointensive care have allowed more precise and earlier diagnoses and more efficient treatments, resulting in improved outcomes. Despite these advances, there is still considerable morbidity and mortality related to these disorders. This aim of this article is to review the current knowledge of the current drugs used in the management of the most important viral encephalitis, focusing on the mechanisms of action, efficacy, and side effects of the drugs. In addition, future perspectives in this area will be addressed. Despite the technological advances, much effort has yet to be undertaken to reduce the impact of these potentially devastating diseases.

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Management of acute viral encephalitis in Brazil

Cited by 16 publications

References 72 publications

Absence of CCR5 increases neutrophil recruitment in severe herpetic encephalitis

Absence of CCR5 increases neutrophil recruitment in severe herpetic encephalitis

Platelet Activating Factor (PAF) Receptor Deletion or Antagonism Attenuates Severe HSV-1 Meningoencephalitis

Viral Encephalitis: Current Treatments and Future Perspectives

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