In Reply: ? Herpes Simplex Virus in Breast Milk

PEDIATRICS ◽  
1979 ◽  
Vol 64 (3) ◽  
pp. 391-391
Author(s):  
Lisa M. Dunkle ◽  
Rose Rita Schmidt ◽  
Dennis M. O'Connor
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Breast Milk ◽  
Herpes Simplex Infection ◽  
Simplex Infection ◽  
Potential Possibility ◽  
The Stability ◽  
Simplex Virus ◽  
Breast Fed

We appreciate Dr. Kibrick's delineation of the stability and infectivity of herpes simplex virus in various media. The remainder of his comments concur with our conclusions and reiterate the potential possibility of risk of herpes simplex infection to some breast-fed infants. The problem would appear to deserve investigation.

scholarly journals Herpes simplex infection as a risk factor for dental caries progression

2012 ◽  
Vol 93 (6) ◽  
pp. 896-899
Author(s):  
J V Andreeva ◽  
A I Bulgakova ◽  
I V Valeev
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Comparison Group ◽  
Clinical Symptoms ◽  
Main Group ◽  
Herpes Simplex Infection ◽  
Simplex Infection ◽  
Diagnodent Pen ◽  
Caries Progression ◽  
Simplex Virus

Aim. To determine the individual risk of caries debut and specific features of the primary caries in patients infected with herpes simplex virus. Methods. 51 patients with primary caries (112 teeth), ICD-10 diagnosis K02.0 (Caries limited to enamel) aged 18 to 49 (female - 42) were examined, all patients were divided into two groups: patients infected with herpes simplex virus and with clinical symptoms of herpes simplex infection (main group, 33 patients), patients infected with herpes simplex virus and without any clinical symptoms of herpes simplex infection (comparison group, 18 patients). Clinical, biochemical, immunological, laser (laser fluorescence spectroscopy) diagnostic techniques were applied. Results. High titers of blood immunoglobulin G to herpes simplex virus were found in 98% of patients examined with initial caries (K02.0). The medium risk was defined in 45% of patients of the main group and in 44% of the comparison group. The navy blue indicator color was the sign of the high risk in 49% in the control group and in 50% of the comparison group. Among the patients with high risk of caries debut the mean local enamel demineralization value according to DIAGNOdent pen was 11.5±1.6 (main group) versus 7.2±1.2 (comparison group). Conclusions. The risk of further caries progression in patients with clinical manifestations of herpes simplex infection is higher compared to patients with persistent infection without signs of active virus reproduction. Biochemical rapid test Clinpro Cario L-Pop (3M ESPE) helps to obtain objective data on oral microflora activity. The use of KaVo «DIAGNOdent pen» device is necessary for the further monitoring of caries progression.

KAPOSI'S VARICELLIFORM ERUPTION; A PRIMARY INFECTION WITH HERPES SIMPLEX VIRUS

PEDIATRICS ◽  
1948 ◽  
Vol 1 (3) ◽  
pp. 364-371
Author(s):  
ISAAC RUCHMAN ◽  
KATHARINE DODD
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Acute Phase ◽  
Primary Infection ◽  
Herpes Simplex Infection ◽  
Simplex Infection ◽  
Control Serum ◽  
Corroborative Evidence ◽  
Neutralization Index ◽  
Simplex Virus

Five cases of Kaposi's varicelliform eruption are reported of which three were children and two were adults. The patients had been exposed to one or more members of the immediate family who had herpes simplex infection. The virus of herpes simplex was recovered from two children and one adult. In all five cases the neutralization index of their sera against herpes virus, little higher than that of control serum during the acute phase of their illness, rose during convalescence. Corroborative evidence is obtained from a study of the above cases that Kaposi's varicelliform eruption is in all probability a manifestation of primary infection with herpes simplex virus in persons with eczema.

Neonatal Herpes Simplex Infection Possibly Acquired via Maternal Breast Milk

PEDIATRICS ◽  
1979 ◽  
Vol 63 (2) ◽  
pp. 250-251
Author(s):  
Lisa M. Dunkle ◽  
Rose Rita Schmidt ◽  
Dennis M. O'Connor
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Breast Milk ◽  
Neonatal Herpes ◽  
Simplex Infection ◽  
History Of ◽  
Neonatal Herpes Simplex ◽  
Simplex Virus ◽  
Hsv 1

A newborn infant with disseminated herpes simplex virus type 1 (HSV-1) infection was determined serologicallv to have acquired the infection postnatally; his mother was found to have HSV-1 in her breast milk but had no history of genital lesions and negative viral cultures of cervix, vagina, and throat. We suggest that HSV-infected maternal breast milk may be a source of this infection for susceptible infants.

scholarly journals cGAS-mediated stabilization of IFI16 promotes innate signaling during herpes simplex virus infection

2015 ◽  
Vol 112 (14) ◽  
pp. E1773-E1781 ◽  
Author(s):  
Megan H. Orzalli ◽  
Nicole M. Broekema ◽  
Benjamin A. Diner ◽  
Dustin C. Hancks ◽  
Nels C. Elde ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Human Fibroblasts ◽  
Interferon Γ ◽  
Viral Dna ◽  
Human Foreskin Fibroblasts ◽  
Infected Cells ◽  
Inducible Protein ◽  
The Stability ◽  
Simplex Virus

Interferon γ-inducible protein 16 (IFI16) and cGMP-AMP synthase (cGAS) have both been proposed to detect herpesviral DNA directly in herpes simplex virus (HSV)-infected cells and initiate interferon regulatory factor-3 signaling, but it has been unclear how two DNA sensors could both be required for this response. We therefore investigated their relative roles in human foreskin fibroblasts (HFFs) infected with HSV or transfected with plasmid DNA. siRNA depletion studies showed that both are required for the production of IFN in infected HFFs. We found that cGAS shows low production of cGMP-AMP in infected cells, but instead cGAS is partially nuclear in normal human fibroblasts and keratinocytes, interacts with IFI16 in fibroblasts, and promotes the stability of IFI16. IFI16 is associated with viral DNA and targets to viral genome complexes, consistent with it interacting directly with viral DNA. Our results demonstrate that IFI16 and cGAS cooperate in a novel way to sense nuclear herpesviral DNA and initiate innate signaling.

scholarly journals What is the True Etiology of “Recurrent Shingles”?

2021 ◽  
Vol 5 (1) ◽  
pp. 7-12
Author(s):  
Ramya Vangipuram ◽  
Harrison Nguyen ◽  
Stephen Tyring
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Zoster ◽  
Herpes Simplex ◽  
Varicella Zoster Virus ◽  
Varicella Zoster ◽  
Dermatology Clinic ◽  
Simplex Infection ◽  
Common Diagnosis ◽  
Recurrent Herpes ◽  
Simplex Virus

Purpose:  To determine the true etiology of cases of putative recurrent shingles referred to a dermatology clinic. Methods: A prospective cohort study of patients aged 15-87 years with reported recurrent herpes zoster was conducted. Vesicular fluid and serology for herpes simplex 1, 2, and varicella zoster virus immunoglobulins were obtained from patients presenting with vesicles. Biopsies were obtained from patients with ambiguous presentations. Results:  44 patients (56%) had evidence of herpes simplex virus infection. 32% of patients had positive herpes simplex virus cultures or polymerase chain reaction sequencing, and 24% additional patients were diagnosed with presumptive simplex infection based on elevated antibody titers. 44% of patients had a diagnosis other than zoster or simplex. One individual had a positive viral culture for varicella zoster virus. 99% of patients who presented with suspected recurrent herpes zoster had no definitive evidence of varicella zoster virus reactivation. Conclusions:  The most common diagnosis was herpes simplex infection. Our results suggest that true recurrent shingles in immunocompetent patients is rare.

? Herpes Simplex Virus in Breast Milk

PEDIATRICS ◽  
1979 ◽  
Vol 64 (3) ◽  
pp. 390-391
Author(s):  
Sidney Kibrick
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Breast Milk ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Primary Infection ◽  
Breast Lesions ◽  
Alternate Hypothesis ◽  
Simplex Virus

The article by Dunkle et al (Pediatrics 63:250, 1979) describes a 6-day-old infant with oropharyngeal lesions due to primary infection with herpes simplex virus type 1 (HSV-1). Recovery of the same virus type from breast milk on day 9 suggested that the milk was the source of the infant's infection. An alternate hypothesis, that the infection was acquired during delivery and subsequently colonized the breast, was considered unlikely since the mother had neither genital nor breast lesions.

The stability of herpes simplex virus on vaginal tampons

1979 ◽  
Vol 3 (3) ◽  
pp. 203-206 ◽  
Author(s):  
Martin G. Myers ◽  
Edem E. Ekwo ◽  
Anita K. Pitts
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
The Stability ◽  
Simplex Virus

scholarly journals US3 protein kinase of herpes simplex virus type 2 is required for the stability of the UL46-encoded tegument protein and its association with virus particles

2005 ◽  
Vol 86 (7) ◽  
pp. 1979-1985 ◽  
Author(s):  
Akio Matsuzaki ◽  
Yohei Yamauchi ◽  
Akihisa Kato ◽  
Fumi Goshima ◽  
Yasushi Kawaguchi ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Protein Kinase ◽  
Virus Replication ◽  
Virus Particles ◽  
Infected Cells ◽  
The Stability ◽  
Simplex Virus

The herpes simplex virus (HSV) US3 gene encodes a serine/threonine protein kinase (PK). Although US3 PK is not essential for virus replication in cell culture, it plays an important role in the regulation of apoptosis in infected cells. However, the role of US3 PK in virus replication and pathogenicity is not well understood. The UL46 gene encodes virion tegument phosphoproteins, the properties and functions of which are poorly understood. In this study, it is shown that the UL46 protein of HSV type 2 (HSV-2) is affected strikingly by the presence of US3 PK. In the absence of US3 PK, UL46 protein was quite unstable, being much more susceptible to degradation. UL46 protein was undetectable in the extracellular virions of US3-deficient virus. Moreover, in vitro kinase assays using recombinant US3 PK show that UL46 protein is phosphorylated by the US3 PK, suggesting that UL46 can be a direct substrate for US3 PK in infected cells. Together, these findings shed new light on the physiological functions of US3 PK.

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