Acute Monarticular Arthritis Caused by Herpes Simplex Virus Type I

PEDIATRICS ◽  
1983 ◽  
Vol 72 (6) ◽  
pp. 882-883
Author(s):  
GARY RAMAFEDI ◽  
ROBERT L. MULDOON

Numerous viruses have been described as potential causes of acute arthritides.1-3 Recently, herpes simplex virus (HSV) type I has been implicated as a possible etiologic agent in acute arthritis in adults.4-6 The purpose here is to review evidence of the role of herpes viruses in acute arthritis and to report the isolation of HSV from the synovial fluid of a child with arthritis. CASE REPORT A 6-year-old of Mexican descent was admitted to the hospital because of the acute onset of pain and swelling in her light knee. The patients had been well until four days prior to admission when she developed fever and painful oral lesions.

2015 ◽  
Vol 2015 ◽  
pp. 1-4 ◽  
Author(s):  
Anna Dalton ◽  
Rosalie Grivell

Background.Disseminated herpes simplex virus (HSV) in the neonate is associated with significant morbidity and mortality. Current guidelines recommend caesarean in third-trimester maternal primary genital HSV outbreaks to prevent transmission from mother to fetus. In the premature fetus, however, expectant management is often necessary to reduce morbidity of prematurity. The benefit of performing caesarean after 6 hrs of rupture of membranes (ROM) to reduce maternal-fetal transmission is unclear.Case. A female patient with primary genital HSV type 1 outbreak coinciding with preterm, prelabour rupture of membranes (PPROM) at 30 + 3 weeks’ gestation. An immediate caesarean section was not performed after multidisciplinary team discussion due to the benefits of glucocorticoids on immune complications of prematurity. The patient had expectant management for 5 days with intravenous (IV) aciclovir and then delivered an infant vaginally with disseminated neonatal HSV.Conclusion. We address the rare presentation of primary HSV infection associated with PPROM and the dilemma of how to manage these patients given the limited literature. We discuss the role of intrauterine compartment monitoring with amniocentesis, the mode of delivery when ROM has occurred for 120 hours, expectant management to reduce prematurity, and the effectiveness of aciclovir to reduce viral shedding in the prevention of neonatal HSV.


2010 ◽  
Vol 1798 (3) ◽  
pp. 579-591 ◽  
Author(s):  
Stefania Galdiero ◽  
Annarita Falanga ◽  
Giuseppe Vitiello ◽  
Mariateresa Vitiello ◽  
Carlo Pedone ◽  
...  

2001 ◽  
Vol 120 (5) ◽  
pp. A136-A137
Author(s):  
K TSAMAKIDES ◽  
E PANOTOPOULOU ◽  
D DIMITROULOPOULOS ◽  
M CHRISTOPOULO ◽  
D XINOPOULOS ◽  
...  

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
David Shahnazaryan ◽  
Rana Khalil ◽  
Claire Wynne ◽  
Caroline A. Jefferies ◽  
Joan Ní Gabhann-Dromgoole ◽  
...  

AbstractHerpes simplex keratitis (HSK), caused by herpes simplex virus type 1 (HSV-1) infection, is the commonest cause of infectious blindness in the developed world. Following infection the virus is initially suspended in the tear film, where it encounters a multi-pronged immune response comprising enzymes, complement, immunoglobulins and crucially, a range of anti-viral and pro-inflammatory cytokines. However, given that HSV-1 can overcome innate immune responses to establish lifelong latency throughout a susceptible individual’s lifetime, there is significant interest in understanding the mechanisms employed by HSV-1 to downregulate the anti-viral type I interferon (IFN) mediated immune responses. This study aimed to investigate the interactions between infected cell protein (ICP)0 and key elements of the IFN pathway to identify possible novel targets that contribute to viral immune evasion. Reporter gene assays demonstrated the ability of ICP0 to inhibit type I IFN activity downstream of pathogen recognition receptors (PRRs) which are known to be involved in host antiviral defences. Further experiments identified interferon regulatory factor (IRF)7, a driver of type I IFN, as a potential target for ICP0. These findings increase our understanding of the pathogenesis of HSK and suggest IRF7 as a potential therapeutic target.


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