1. Clin Rheumatol. 2010 Mar 1. [Epub ahead of print]

Wegener's granulomatosis: experience from a Brazilian tertiary center.

de Souza FH, Radu Halpern AS, Valente Barbas CS, Shinjo SK.

Division of Rheumatology, Faculdade de Medicina da Universidade de São Paulo, Av.
Dr. Arnaldo, 455, 3 degrees andar, Sala 3190, CEP 01246-903, São Paulo, Brazil.

Most epidemiological studies with Wegener's granulomatosis (WG) patients are
based on populations from the Northern hemisphere, whereas very few studies have 
been conducted in Southern hemisphere populations, particularly from South
America. The authors performed a large retrospective, demographic study including
clinical and laboratory profiles of 134 consecutive WG patients seen at one
Brazilian center from 1999 to 2009. Mean age at initial WG diagnosis was 43.4 +/-
15.5 years, and mean disease duration was 8.6 +/- 6.6 years. Sixty-four (47.8%)
patients were male and a total of 113 (84.3%) subjects were white.
Ear/nose/throat involvement occurred in 85.8%. The classic lung and renal
involvement were observed in 77.6% and 75.4%, respectively, followed by ocular
(35.8%), musculoskeletal (33.4%), cutaneous (29.1%), neurological (20.1%),
cardiac (11.2%), and genitourinary involvement in 2.2% of cases. Cytoplasmic
pattern-antineutrophil cytoplasmic antibody was detected in 83 (61.9%) cases. Ten
(7.5%) individuals presented limited forms of WG. Classic therapy with
corticosteroids and cyclophosphamide was used in 97 cases (72.4%). There were no 
cases of tuberculosis or Pneumocystis jiroveci pneumonia, but cutaneous herpes
zoster occurred in eight (6.0%) individuals. There were 29 deaths (21.6%).
Eighteen patients died of septic shock (mainly bacterial pneumonia), whereas four
died of alveolar hemorrhage, four of myocardial infarction, and three of other
causes. In summary, our data from a very large retrospective and descriptive
study mirrored the main clinical features of WG described in other countries,
demonstrating that they may serve as a reference for South American populations.

PMID: 20195878 [PubMed - as supplied by publisher]


2. Pediatrics. 2010 Mar 1. [Epub ahead of print]

Vaccine-associated Herpes Zoster Opthalmicus and Encephalitis in an
Immunocompetent Child.

Chouliaras G, Spoulou V, Quinlivan M, Breuer J, Theodoridou M.

First Department of Pediatrics, University of Athens, "Aghia Sophia" Children's
Hospital, Thivon & Levadias, Athens, Greece; and.

Varicella-zoster virus vaccine has diminished the consequences of chicken pox in 
terms of health and economical burden. The increasing number of doses
administered worldwide has revealed rare but important adverse effects that had
not occurred during clinical trials. We report here the case of an
immunocompetent 3(1/2)-year-old girl who developed encephalitis and herpes zoster
opthalmicus 20 months after her immunization with varicella-zoster virus vaccine.
Molecular analysis confirmed the vaccine strain as the causative agent. After an 
intravenous course with acyclovir, the child made a full recovery with no
neurologic sequelae.

PMID: 20194287 [PubMed - as supplied by publisher]


3. J Acquir Immune Defic Syndr. 2010 Mar 1;53(3):417-8.

Herpes Zoster Among HIV-Infected Patients in the Highly Active Antiretroviral
Therapy Era: Korean HIV Cohort Study.

Song JY, Lee JS, Jung HW, Choi HJ, Lee JS, Eom JS, Cheong HJ, Jung MH, Kim WJ.

*Division of Infectious Diseases, Department of Internal Medicine, Korea
University College of Medicine, Seoul, Korea; daggerInha University College of
Medicine, Incheon, Korea; double daggerChungbuk National University College of
Medicine, Cheongju, Korea; section signEwha University College of Medicine,
Seoul, Korea; ||Hallym University College of Medicine, Seoul, Korea.

PMID: 20190589 [PubMed - in process]


4. Curr Top Microbiol Immunol. 2010 Feb 26. [Epub ahead of print]

Molecular Characterization of Varicella Zoster Virus in Latently Infected Human
Ganglia: Physical State and Abundance of VZV DNA, Quantitation of Viral
Transcripts and Detection of VZV-Specific Proteins.

Azarkh Y, Gilden D, Cohrs RJ.

Departments of Neurology (Y.A., D.G., R.J.C.) and Microbiology (D.G.), University
of Colorado Denver School of Medicine, 12700 E. 19th Avenue, Mail Stop B182,
Aurora, CO, 80045, USA.

Varicella zoster virus (VZV) establishes latency in neurons of human peripheral
ganglia where the virus genome is most likely maintained as a circular episome
bound to histones. There is considerable variability among individuals in the
number of latent VZV DNA copies. The VZV DNA burden does not appear to exceed
that of herpes simplex type 1 (HSV-1). Expression of VZV genes during latency is 
highly restricted and is regulated epigenetically. Of the VZV open reading frames
(ORFs) that have been analyzed for transcription during latency using cDNA
sequencing, only ORFs 21, 29, 62, 63, and 66 have been detected. VZV ORF 63 is
the most frequently and abundantly transcribed VZV gene detected in human ganglia
during latency, suggesting a critical role for this gene in maintaining the
latent state and perhaps the early stages of virus reactivation. The inconsistent
detection and low abundance of other VZV transcripts suggest that these genes
play secondary roles in latency or possibly reflect a subpopulation of neurons
undergoing VZV reactivation. New technologies, such as GeXPS multiplex PCR, have 
the sensitivity to detect multiple low abundance transcripts and thus provide a
means to elucidate the entire VZV transcriptome during latency.

PMID: 20186615 [PubMed - as supplied by publisher]


5. Curr Top Microbiol Immunol. 2010 Feb 26. [Epub ahead of print]

Neurological Disease Produced by Varicella Zoster Virus Reactivation Without
Rash.

Gilden D, Cohrs RJ, Mahalingam R, Nagel MA.

Departments of Neurology (D.G., R.J.C., R.M., M.A.N.) and Microbiology (D.G.),
University of Colorado Denver School of Medicine, 12700 E. 19th Avenue, Mail Stop
B182, Aurora, CO, 80045, USA, don.gilden@ucdenver.edu.

Reactivation of varicella zoster virus (VZV) from latently infected human ganglia
usually produces herpes zoster (shingles), characterized by dermatomal
distribution pain and rash. Zoster is often followed by chronic pain
(postherpetic neuralgia or PHN) as well as meningitis or meningoencephalitis,
cerebellitis, isolated cranial nerve palsies that produce ophthalmoplegia or the 
Ramsay Hunt syndrome, multiple cranial nerve palsies (polyneuritis cranialis),
vasculopathy, myelopathy, and various inflammatory disorders of the eye.
Importantly, VZV reactivation can produce chronic radicular pain without rash
(zoster sine herpete), as well as all the neurological disorders listed above
without rash. The protean neurological and ocular disorders produced by VZV in
the absence of rash are a challenge to the practicing clinician. The presentation
of these conditions varies from acute to subacute to chronic. Virological
confirmation requires the demonstration of amplifiable VZV DNA in cerebrospinal
fluid (CSF) or in blood mononuclear cells, or the presence of anti-VZV IgG
antibody in CSF or of anti-VZV IgM antibody in CSF or serum.

PMID: 20186614 [PubMed - as supplied by publisher]


6. Curr Top Microbiol Immunol. 2010 Feb 26. [Epub ahead of print]

VZV ORF47 Serine Protein Kinase and Its Viral Substrates.

Kenyon TK, Grose C.

Department of Pediatrics/2501 JCP, University of Iowa Hospital, Iowa City, IA,
52242, USA.

ORF47, a serine protein kinase of varicella-zoster virus (VZV) and homolog of
herpes simplex virus UL13, is an interesting modulator of VZV pathogenesis. This 
chapter summarizes research showing that ORF47 protein kinase activity, by virtue
of phosphorylation of or binding to various viral substrates, regulates VZV
proteins during all phases of viral infection and has a pronounced effect on the 
trafficking of gE, the predominant VZV glycoprotein, which in turn is critical
for cell-to-cell spread of the virus. Casein kinase II, an ubiquitous cellular
protein kinase, recognizes a similar but less stringent phosphorylation consensus
sequence and can partially compensate for lack of ORF47 activity in VZV-infected 
cells. Differences between the phosphorylation consensus sites of the viral and
cellular kinases are outlined in detail.

PMID: 20186612 [PubMed - as supplied by publisher]


7. Am J Med Sci. 2010 Feb 24. [Epub ahead of print]

Viruses and Arthritis: New Challenges in Diagnosis, Therapy, and Immunization.

Reimold A.

From the Rheumatic Diseases Division, University of Texas Southwestern Medical
Center and Dallas VA Medical Center, Dallas, Texas.

BACKGROUND:: Althoughmany viruses produce musculoskeletal symptoms during an
acute infection, a long-term inflammatory arthritis remains an unusual
consequence. When evaluating arthritis in a patient with a chronic or latent
viral infection, serologic testing and therapeutic options are significantly
altered. RESULTS:: The example of hepatitis C reveals how chronic infection can
complicate the diagnosis of rheumatoid arthritis. Determination of rheumatoid
factor is of limited utility, whereas the anticyclic citrullinated peptide has
become a new test with improved specificity. Therapeutic options are severely
constrained because of potential hepatotoxicity of oral agents such as
methotrexate and leflunomide. Antitumor necrosis factor alpha biologics have
demonstrated initial safety in the setting of hepatitis C virus but may be
associated with reactivation of hepatitis B virus. Biologics such as abatacept
and rituximab have been inadequately studied in this population to date.
Prevention of viral infections by influenza and herpes zoster vaccines in
rheumatoid arthritis patients needs improved administration rates and careful
planning to maximize efficacy. CONCLUSIONS:: Chronic viral infections complicate 
the diagnosis and therapy of inflammatory arthritis. The antitumor necrosis
factor alpha biologics have become important therapeutic options for patients
with hepatitis C. Vaccination against influenza and herpes zoster are underused
in health maintenance of arthritis patients.

PMID: 20186043 [PubMed - as supplied by publisher]


8. J Natl Cancer Inst. 2010 Feb 24. [Epub ahead of print]

Immune-Related and Inflammatory Conditions and Risk of Lymphoplasmacytic Lymphoma
or Waldenstrom Macroglobulinemia.

Kristinsson SY, Koshiol J, Björkholm M, Goldin LR, McMaster ML, Turesson I,
Landgren O.

Affiliations of authors: Department of Medicine, Division of Hematology,
Karolinska University Hospital Solna and Karolinska Institutet, Stockholm, Sweden
(SYK, OL); Genetic Epidemiology Branch, Division of Cancer Epidemiology and
Genetics (JK, LRG, MLM, OL) and Center for Cancer Research (OL), National Cancer 
Institute, National Institutes of Health, Bethesda, MD; Department of Medicine,
Section of Hematology, Malmö University Hospital, Malmö, Sweden (IT).

Background Chronic immune stimulation appears to be associated with
lymphoplasmacytic lymphoma (LPL)-Waldenström macroglobulinemia (WM); however,
available information is sparse. We conducted, to our knowledge, the most
comprehensive study to date to evaluate associations between a personal or family
history of many immune-related and/or inflammatory disorders and the subsequent
risk of LPL-WM. Methods We used Swedish population-based registries to identify
2470 case patients with LPL-WM, 9698 matched control subjects, and almost 30 000 
first-degree relatives of either case patients or control subjects. We evaluated 
a wide range of autoimmune, infectious, allergic, and inflammatory conditions. We
calculated odds ratios (ORs) and 95% confidence intervals (CIs) for each
condition by use of logistic regression. Results An increased risk of LPL-WM was 
associated with a personal history of the following autoimmune diseases: systemic
sclerosis (OR = 4.7, 95% CI = 1.4 to 15.3), Sjögren syndrome (OR = 12.1, 95% CI =
3.3 to 45.0), autoimmune hemolytic anemia (OR = 24.2, 95% CI = 5.4 to 108.2),
polymyalgia rheumatica (OR = 2.9, 95% CI = 1.6 to 5.2), and giant cell arteritis 
(OR = 8.3, 95% CI = 2.1 to 33.1). An increased risk of LPL-WM was associated with
a personal history of the following infectious diseases: pneumonia (OR = 1.4, 95%
CI = 1.1 to 1.7), septicemia (OR = 2.4, 95% CI = 1.2 to 4.3), pyelonephritis (OR 
= 1.7, 95% CI = 1.1 to 2.5), sinusitis (OR = 2.7, 95% CI = 1.4 to 4.9), herpes
zoster (OR = 3.4, 95% CI = 2.0 to 5.6), and influenza (OR = 2.9, 95% CI = 1.7 to 
5.0). An increased risk of LPL-WM was associated with a family history of the
following autoimmune or infectious diseases: Sjögren syndrome (OR = 5.0, 95% CI =
2.1 to 12.0), autoimmune hemolytic anemia (OR = 3.8, 95% CI = 1.1 to 13.2),
Guillain-Barré syndrome (OR = 4.1, 95% CI = 1.8 to 9.4), cytomegalovirus (OR =
2.7, 95% CI = 1.4 to 5.3), gingivitis and periodontitis (OR = 1.9, 95% CI = 1.3
to 2.7), and chronic prostatitis (OR = 4.3, 95% CI = 1.7 to 11.1). Conclusions
Personal history of certain immune-related and/or infectious conditions was
strongly associated with increased risk of LPL-WM. The association of both
personal and family history of Sjögren syndrome and autoimmune hemolytic anemia
with risk of LPL-WM indicates the potential for shared susceptibility for these
conditions.

PMID: 20181958 [PubMed - as supplied by publisher]


9. J Clin Virol. 2010 Feb 22. [Epub ahead of print]

Disease burden of herpes zoster in Korea.

Choi WS, Noh JY, Huh JY, Jo YM, Lee J, Song JY, Kim WJ, Cheong HJ.

Division of Infectious Disease, Department of Internal Medicine, Korea University
College of Medicine, Seoul, Republic of Korea.

BACKGROUND: The occurrence of herpes zoster can deteriorate the quality of life
considerably, resulting in high disease burden. While Korea is assumed to have
high disease burden of herpes zoster, there has been no researches analyzing
this. OBJECTIVES: We performed this study to investigate the disease burden of
herpes zoster in the Korean population as a whole. STUDY DESIGN: We used the
database of the Health Insurance Review & Assessment Service of Korea and
analyzed the data of patients who had herpes zoster as a principal diagnosis
during the period from 2003 to 2007. We investigated the annual prevalence, rate 
of clinical visits, rate of hospitalization, and the pattern of medical services 
use. The socioeconomic burden of herpes zoster was calculated by a conversion
into cost. RESULTS: Rates of clinic visits and hospitalizations due to herpes
zoster during the 5-year period from 2003 to 2007 were 7.93-12.54 per 1000
population and 0.22-0.32 per 1000 population, respectively. Prevalence rates
according to age increased sharply after 50 years and reached a peak at 70 years.
The total socioeconomic cost of herpes zoster was $75.9-143.8 million per year,
increasing every year by 14-20%. CONCLUSIONS: There is a heavy socioeconomic
burden due to herpes zoster in Korea and indicate that appropriate policies need 
to be established to reduce this burden. Additional researches are also necessary
to assess the safety, efficacy and cost-effectiveness of a herpes zoster vaccine 
in the Korean population. Copyright © 2010 Elsevier B.V. All rights reserved.

PMID: 20181512 [PubMed - as supplied by publisher]


10. Cases J. 2010 Jan 12;3(1):17.

An unusual cause of visual loss after Herpes zoster ophthalmicus: a case report.

Camuglia JE, Beltz JE, Khurana K, Hall AJ.

Department of Ophthalmology, The Alfred Hospital, Commercial Road, Prahran,
Melbourne, Victoria 3004, Australia. hall@eyesurgery.com.au.

ABSTRACT: INTRODUCTION: The vascular complications of herpes zoster are well
recognised, however, there are few reports of central retinal artery occlusion.
Central retinal artery occlusion following herpes zoster ophthalmicus is poorly
recognised. This is likely due to the difficulties in obtaining tissue for
histopathology to establish causality. We report a case of central retinal artery
occlusion and complete internal carotid artery occlusion following herpes zoster 
ophthalmicus. CASE PRESENTATION: A 44 year old Caucasian female presented with
sudden painless loss of vision in her right eye on a background of chronic
lymphocytic leukaemia and right sided herpes zoster ophthalmicus. She was
initially treated with steroids and antivirals for an underlying presumed
vasculitic cause, but review at 24 hours demonstrated a right central retinal
artery occlusion. Embolic screen identified complete occlusion of the right
internal carotid artery. She was treated with oral antiviral medication for three
weeks but had no visual recovery. CONCLUSION: This case highlights an uncommon
cause of acute visual loss. We propose that the underlying small and large vessel
occlusion in this patient was due to herpes zoster related vasculopathy. A review
of the literature is presented to trace the historical perspective of herpes
zoster related vasculopathy.

PMCID: PMC2829517
PMID: 20180950 [PubMed - in process]


11. Clin Infect Dis. 2010 Feb 23. [Epub ahead of print]

Increasing Incidence of Herpes Zoster among Veterans.

Rimland D, Moanna A.

Atlanta Veterans Affairs Medical Center, Decatur, and 2Emory University School of
Medicine, Atlanta, Georgia.

Background. The incidence of herpes zoster in the United States has been
estimated to be 1 million cases annually, with a higher rate in adults older than
60 years. The morbidity of the disease, including postherpetic neuralgia, imposes
significant effects on quality of life. We analyzed reports of herpes zoster in
the Veterans Affairs (VA) population because these patients are older and could
provide a reflection of disease trends in the aging US population. These data
will provide a baseline for future analyses of the incidence of herpes zoster
after the introduction of the herpes zoster vaccine in late 2007. Methods. To
evaluate the trend in the annual incidence of herpes zoster for fiscal year 2000 
(beginning October 1999) through fiscal year 2007 (through September 2007), we
derived incidence rates using the Veterans Health Administration Decision Support
System reports of herpes zoster by International Classification of Diseases,
Ninth Revision codes from 2000 through 2007 and the corresponding denominator
data for all veterans in care. These rates were validated by review of medical
records of patients with diagnoses of herpes zoster at the Atlanta VA Medical
Center. Results. The annual incidence of herpes zoster increased from 3.10
episodes per 1000 veterans in 2000 to 5.22 in 2007 ([Formula: see text];
[Formula: see text]). This increasing rate was seen in both men and women but
only in groups older than 40 years. Conclusion. The increasing incidence of
herpes zoster in our veteran population and its effect on the quality of life of 
the veterans validate the need for improved rates of vaccination in this
population.

PMID: 20178416 [PubMed - as supplied by publisher]


12. J Clin Oncol. 2010 Feb 22. [Epub ahead of print]

Phase I Study of KW-0761, a Defucosylated Humanized Anti-CCR4 Antibody, in
Relapsed Patients With Adult T-Cell Leukemia-Lymphoma and Peripheral T-Cell
Lymphoma.

Yamamoto K, Utsunomiya A, Tobinai K, Tsukasaki K, Uike N, Uozumi K, Yamaguchi K, 
Yamada Y, Hanada S, Tamura K, Nakamura S, Inagaki H, Ohshima K, Kiyoi H, Ishida
T, Matsushima K, Akinaga S, Ogura M, Tomonaga M, Ueda R.

Department of Hematology and Cell Therapy, Aichi Cancer Center; Department of
Clinical Pathophysiology and Department of Infectious Diseases, Nagoya University
Graduate School of Medicine; Department of Hematology and Oncology, Nagoya Daini 
Red Cross Hospital, Nagoya; Department of Clinical Pathology and Department of
Medical Oncology and Immunology, Nagoya City University Graduate School of
Medical Sciences, Nagaya; Department of Hematology, Imamura Bun-in Hospital;
Department of Internal Medicine, National Hospital Organization Kagoshima Medical
Center; Department of Hematology and Immunology, Kagoshima University Hospital,
Kagoshima; Hematology and Stem Cell Transplantation Division, National Cancer
Center Hospital; Department of Safety Research on Blood and Biologics, National
Institute of Infectious Diseases; Department of Molecular Preventive Medicine,
Graduate School of Medicine, The University of Tokyo; Kyowa Hakko Kirin Co Ltd,
Tokyo; Department of Hematology and Molecular Medicine Unit and Department of
Laboratory Medicine, Nagasaki University Graduate School of Biomedical Science,
Nagasaki; Department of Hematology, National Kyushu Cancer Center; The Department
of Medicine, Division of Medical Oncology, Infectious Disease, and Endocrinology,
School of Medicine, Fukuoka University, Fukuoka; and the Department of
Pathophysiology, Kurume University School of Medicine, Kurume, Japan.

PURPOSE: KW-0761, a defucosylated humanized anti-CC chemokine receptor 4 (CCR4)
antibody, exerts a strong antibody-dependent cellular cytotoxic effect. This
phase I study assessed the safety, pharmacokinetics, recommended phase II dose
and efficacy of KW-0761 in patients with relapsed CCR4-positive adult T-cell
leukemia-lymphoma (ATL) or peripheral T-cell lymphoma (PTCL). PATIENTS AND
METHODS: Sixteen patients received KW-0761 once a week for 4 weeks by intravenous
infusion. Doses were escalated, starting at 0.01, 0.1, 0.5, and finally 1.0 mg/kg
by a 3 + 3 design. RESULTS: Fifteen patients completed the protocol treatment.
Only one patient, at the 1.0 mg/kg dose, developed grade 3 dose-limiting
toxicities, skin rash, and febrile neutropenia, and grade 4 neutropenia. Other
treatment-related grade 3 to 4 toxicities were lymphopenia (n = 10), neutropenia 
(n = 3), leukopenia (n = 2), herpes zoster (n = 1), and acute infusion
reaction/cytokine release syndrome (n = 1). Neither the frequency nor severity of
toxicities increased with dose escalation. The maximum tolerated dose was not
reached. Therefore, the recommended phase II dose was determined to be 1.0 mg/kg.
No patients had detectable levels of anti-KW-0761 antibody. The plasma maximum
and trough, and the area under the curve of 0 to 7 days of KW-0761, tended to
increase dose and frequency dependently. Five patients (31%; 95% CI, 11% to 59%) 
achieved objective responses: two complete (0.1; 1.0 mg/kg) and three partial
(0.01; 2 at 1.0 mg/kg) responses. CONCLUSION: KW-0761 was tolerated at all the
dose levels tested, demonstrating potential efficacy against relapsed
CCR4-positive ATL or PTCL. Subsequent phase II studies at the 1.0 mg/kg dose are 
thus warranted.

PMID: 20177026 [PubMed - as supplied by publisher]


13. Aliment Pharmacol Ther. 2010 Feb 18. [Epub ahead of print]

Infliximab as rescue medication for patients with severe ulcerative/indeterminate
colitis refractory to tacrolimus.

Herrlinger KR, Barthel DN, Schmidt KJ, Büning J, Barthel CS, Wehkamp J, Stange
EF, Fellermann K.

Department of Gastroenterology, Hepatology and Endocrinology,
Robert-Bosch-Hospital, Stuttgart, Germany.

SUMMARY Background: The calcineurin inhibitor tacrolimus and the
anti-TNF-antibody infliximab are established options in steroid refractory
ulcerative colitis (UC). The aim of this study was to determine the efficacy of
infliximab as rescue medication in patients failing to respond to tacrolimus.
Aim: To evaluate the efficacy of infliximab-salvage therapy in patients with
refractory ulcerative colitis failing to respond to tacrolimus Methods:
Twenty-four patients were enrolled in this evaluation. Reasons for tacrolimus
therapy were steroid-refractory disease in 19 patients and steroid dependency in 
5 patients. All patients receiving infliximab had tacrolimus refractory active
disease (Lichtiger score >10) and were treated with 5mg/kg at weeks 0, 2 and 6
and every 8 weeks thereafter if tolerated. Results: Six of 24 patients (25%)
achieved remission following infliximab infusion and 4/24 (17%) had an initial
response only but underwent proctocolectomy later due to loss of response (3) or 
development of a delayed hypersensitivity reaction (1). Fourteen patients (58%)
completely failed to respond with 10 undergoing colectomy. Eight patients
experienced side effects under infliximab including two infectious complications 
(herpes zoster and herpes pneumonia). Conclusions: Infliximab offers a
therapeutic option as rescue therapy in about a quarter of patients with active
UC after failing to respond to tacrolimus. This benefit has to be weighed against
the risks of infectious complications.

PMID: 20175769 [PubMed - as supplied by publisher]


14. J Pharmacol Sci. 2010 Feb 20. [Epub ahead of print]

Blockade of Glycine Transporter (GlyT) 2, but Not GlyT1, Ameliorates Dynamic and 
Static Mechanical Allodynia in Mice With Herpetic or Postherpetic Pain.

Nishikawa Y, Sasaki A, Kuraishi Y.

Department of Applied Pharmacology, Graduate School of Medicine and
Pharmaceutical Sciences, University of Toyama, Japan.

Glycine is an inhibitory neurotransmitter in the spinal dorsal horn and its
extracellular concentration is regulated by glial glycine transporter (GlyT) 1
and neuronal GlyT2. This study was conducted to elucidate the effects of
intrathecal injections of GlyT1 and GlyT2 inhibitors on two distinct types of
mechanical allodynia, dynamic and static allodynia, in mice with herpetic or
postherpetic pain. The GlyT2 inhibitor ALX1393, but not the GlyT1 inhibitor
sarcosine, suppressed dynamic and static allodynia at the herpetic and
postherpetic stages. Intrathecal ALX1393 suppressed dynamic allodynia induced by 
intrathecal strychnine and N-methyl-D-aspartate (NMDA). Intrathecal sarcosine
suppressed dynamic allodynia induced by intrathecal strychnine, but not NMDA.
Expression level of GlyT1, but not GlyT2, mRNA in the lumbar dorsal horn was
decreased at the herpetic and postherpetic stages. Glycine receptor
alpha1-subunit mRNA was decreased in the lumbar dorsal horn at the herpetic, but 
not postherpetic stage, without alteration in alpha3-subunit mRNA. The results
suggest that GlyT2 is a potential target for treatment of dynamic and static
allodynia in patients with herpes zoster and postherpetic neuralgia. The lack of 
efficacy of GlyT1 inhibitor may be explained by activation of NMDA receptors and 
the down-regulation of GlyT1 in the lumbar dorsal horn.

PMID: 20173309 [PubMed - as supplied by publisher]


15. J Virol Methods. 2010 Feb 18. [Epub ahead of print]

The glycoproteins C and G are equivalent target antigens for the determination of
herpes simplex virus type 1-specific antibodies.

Scheper T, Saschenbrecker S, Steinhagen K, Sauerbrei A, Suer W, Meyer W,
Schlumberger W, Wandinger KP.

Institute of Experimental Immunology, affiliated to EUROIMMUN AG, Seekamp 31,
D-23560 Luebeck, Germany.

Seroreactivity to the glycoproteins C and G of herpes simplex virus type 1
(HSV-1) was compared in 310 serum samples using a Western blot assay containing a
whole antigen extract of HSV-1 and an ELISA employing gC1 isolated from HSV-1.
The prevalence of reactivity to gC1 was 75.8% by Western blot and 73.9% by ELISA,
while antibody responses to gG1 were detected in 72.9% of sera by Western blot.
An absolute correlation of 96.1% between the reactivity to gC1 and gG1 was
demonstrated using the Western blot. The gC1-based ELISA correlated with Western 
blot detection of anti-gC1 and anti-gG1 antibodies in 95.2 and 97.7% of samples, 
respectively. 3.2% of all sera were reactive with gC1 in Western blot and/or
ELISA, but were negative for anti-gG1. For analysis of cross-reactivity,
antibodies against HSV-2, Epstein-Barr virus, varicella-zoster virus and
cytomegalovirus were determined. The prevalence of antibodies against each
individual virus was identical in the groups of sera reactive with gC1 or gG1.
These findings indicate that gC1 and gG1 are equivalent antigenic targets for the
type-specific serodiagnosis of HSV-1 infections. Copyright © 2010. Published by
Elsevier B.V.

PMID: 20171247 [PubMed - as supplied by publisher]


16. Hautarzt. 2010 Feb 19. [Epub ahead of print]

[Skin infections after transplantation.]

[Article in German]

Wolf IH.

Universitätsklinik für Dermatologie und Venerologie, Abteilung für Allgemeine
Dermatologie, Medizinische Universität Graz, Auenbruggerplatz 8, 8036, Graz,
Osterreich, ingrid.wolf@medunigraz.at.

Skin infections after transplantation are frequent and of special importance
because they may be quite severe. The spectrum of dermatologic infections in
transplant recipients includes bacterial, mycotic and viral diseases. Pyoderma,
herpes virus 6/7, herpes simplex virus, varicella-zoster virus, cytomegalovirus
and candida infections predominate. Rare pathogens must be also considered.
Cutaneous infections can be divided into three phases following transplantation. 
Diagnosis and adequate early therapy together with specific prophylaxis and
follow-up of transplant patients should be strived for to avoid life-threatening 
complications.

PMID: 20165826 [PubMed - as supplied by publisher]


17. Arch Phys Med Rehabil. 2010 Feb;91(2):321-5.

Herpes zoster-induced trunk muscle paresis presenting with abdominal wall
pseudohernia, scoliosis, and gait disturbance and its rehabilitation: a case
report.

Tashiro S, Akaboshi K, Kobayashi Y, Mori T, Nagata M, Liu M.

Department of Rehabilitation Medicine, Ichikawa City Rehabilitation Hospital,
Ichikawa City, Japan. s-tashiro@umin.net

Herpes zoster (HZ)-induced abdominal wall pseudohernia has been frequently
reported, but there has been no report describing HZ-induced trunk muscle paresis
leading to functional problems. We describe a 73-year-old man with T12 and L1
segmental paresis caused by HZ presenting with abdominal wall pseudohernia,
scoliosis, and standing and gait disturbance who responded well to a systematic
rehabilitation approach. He first noticed a right abdominal bulge in the 6th
postherpetic week, which was gradually accompanied by right convex thoracolumbar 
scoliosis, pain, and standing and gait disturbance in the 12th week. Needle
electromyography revealed abnormal spontaneous activities at rest in the right
T12 myotomal muscles, and motor unit recruitment was markedly decreased. We
arranged an outpatient rehabilitation program consisting of using a soft
thoracolumbosacral orthosis for pain relief and trunk stability, muscle
reeducation of the paretic abdominal muscles, strengthening of the disused trunk 
and extremity muscles, and gait exercise. Based on electromyographic findings, we
instructed him in an effective method of muscle reeducation. After 4 months of
rehabilitation, he showed marked improvement and became an outdoor ambulator. We 
suggest that electromyography is a useful tool to evaluate clinical status and
devise an effective rehabilitation program in patients with HZ trunk paresis.
Copyright 2010 American Congress of Rehabilitation Medicine. Published by
Elsevier Inc. All rights reserved.

PMID: 20159140 [PubMed - in process]


18. J Neurol. 2010 Feb 13. [Epub ahead of print]

Trigeminal herpes zoster and Ramsay Hunt Syndrome with a lesion in the spinal
trigeminal nucleus and tract.

Hung CW, Wang SJ, Chen SP, Lirng JF, Fuh JL.

Department of Neurology, Yangming Branch, Taipei City Hospital, Taipei, Taiwan,
ROC.

We report the case of a 77-year-old immuno-competent man who developed herpes
zoster in the maxillary and mandibular branches of the trigeminal nerve. Within 3
weeks, he developed ipsilateral peripheral facial palsy, hearing loss, vesicles
over the external auditory canal, and pain in the face and ear. A T(2)-weighted
MRI of the brain revealed a hyper-intense lesion at the right medulla
corresponding to the spinal trigeminal nucleus and tract. Gadolinium enhancement 
was seen over the right facial nerve. These lesions suggest a possibility of
transaxonal spread of the varicella zoster virus between the trigeminal nerve,
the facial nerve, and the spinal trigeminal nucleus and tract.

PMID: 20155276 [PubMed - as supplied by publisher]


19. Nat Rev Rheumatol. 2010 Feb 9. [Epub ahead of print]

Tumor necrosis factor blockade and the risk of viral infection.

Kim SY, Solomon DH.

Division of Rheumatology, Immunology, and Allergy, and Division of
Pharmacoepidemiology and Pharmacoeconomics, Brigham and Women's Hospital, 75
Francis Street, Boston, MA 02115, USA.

Tumor necrosis factor (TNF) blockers are widely used to treat rheumatoid
arthritis and other chronic inflammatory diseases. Many studies have demonstrated
an increased risk of opportunistic infections such as tuberculosis and fungal
infection in patients treated with TNF blockers, which is thought to be related
to the primary role of TNF both in host defense and in the immune response.
Little is known, however, about the association between TNF blockade and the
development of viral infection. Owing to the critical role of TNF in the control 
of viral infection, depletion of this cytokine with TNF blockers could facilitate
the development or reactivation of viral infection. A number of large
observational studies have found an increased risk of herpes zoster in patients
receiving TNF blockers for the treatment of rheumatoid arthritis. This Review
draws attention to the risk of several viral infections, including HIV, varicella
zoster virus, Epstein-Barr virus, cytomegalovirus, and human papillomavirus, in
patients receiving TNF-blocking therapy for chronic inflammatory conditions. In
addition, implications for clinical practice and possible preventative approaches
are discussed.

PMID: 20142812 [PubMed - as supplied by publisher]


20. Proc Natl Acad Sci U S A. 2010 Feb 9;107(6):2461-6. Epub 2010 Jan 21.

Transcriptional coactivator HCF-1 couples the histone chaperone Asf1b to HSV-1
DNA replication components.

Peng H, Nogueira ML, Vogel JL, Kristie TM.

Laboratory of Viral Diseases, National Institute of Allergy and Infectious
Diseases, National Institutes of Health, Bld 4-131, 4 Center Drive, Bethesda, MD 
20892, USA.

The cellular transcriptional coactivator HCF-1 interacts with numerous
transcription factors as well as other coactivators and is a component of
multiple chromatin modulation complexes. The protein is essential for the
expression of the immediate early genes of both herpes simplex virus (HSV) and
varicella zoster virus and functions, in part, by coupling chromatin modification
components including the Set1 or MLL1 histone methyltransferases and the histone 
demethylase LSD1 to promote the installation of positive chromatin marks and the 
activation of viral immediately early gene transcription. Although studies have
investigated the role of HCF-1 in both cellular and viral transcription, little
is known about other processes that the protein may be involved in. Here we
demonstrate that HCF-1 localizes to sites of HSV replication late in infection.
HCF-1 interacts directly and simultaneously with both HSV DNA replication
proteins and the cellular histone chaperone Asf1b, a protein that regulates the
progression of cellular DNA replication forks via chromatin reorganization. Asf1b
localizes with HCF-1 in viral replication foci and depletion of Asf1b results in 
significantly reduced viral DNA accumulation. The results support a model in
which the transcriptional coactivator HCF-1 is a component of the HSV DNA
replication assembly and promotes viral DNA replication by coupling Asf1b to DNA 
replication components. This coupling provides a novel function for HCF-1 and
insights into the mechanisms of modulating chromatin during DNA replication.

PMID: 20133788 [PubMed - in process]