g. interleukin (IL)-12, IL-18 and interferon (IFN)-α]; (iii) APC intrinsic factors such

as differentiation state (e.g. monocyte versus DC) and Toll-like receptor (TLR) stimulation. Together with recent findings that demonstrate new links between NKT cell activation and endogenous lipid metabolism, these results outline a picture in which the functions of NKT cells are closely attuned to the existing biological context. Thus, NKT cells may actively promote tolerance until a critical level of danger signals arises, SB203580 mw at which point they switch to activating pro-inflammatory immune responses. Natural killer T (NKT) cells were first identified as a small population of T cells in naïve mice that

express CD161 (also called NK1.1 or NKR-P1A), a marker that is characteristic of natural killer (NK) cells.1 It subsequently became clear that most of these T cells are restricted by CD1d, a non-classical type of antigen-presenting molecule with structural similarity to major histocompatibility complex (MHC) class I proteins.2,3 Further studies have revealed that, while NKT cells often express NK receptors, these are not specific lineage markers for CD1d-restricted T cells.4,5 Moreover, while NKT cells share some functional and gene expression patterns with NK cells and cytotoxic T lymphocytes (CTLs), they also have many prominent features that are more frequently associated with helper T cells.6–8 Thus, Akt inhibitor in vivo while NKT cells are an innate

T lymphocyte population, the implication from their name that they function predominantly as cytolytic effectors is not entirely accurate. Instead, a number of observations suggest that a major role of NKT cells is to serve as a type of regulatory T cell that can drive downstream immune responses along either pro-inflammatory or silencing pathways. Support for this view comes from findings that NKT cells produce a wide variety of cytokines, including both T helper type 1 (Th1) and Th2 types; that mice genetically deficient in NKT cells show defects not only in resistance to microbial Endonuclease infections and in tumour immunosurveillance but also in establishing peripheral tolerance and preventing autoimmunity; and that specific activation of NKT cells in vivo can inhibit the onset of autoimmune diseases as well as promote microbial clearance or tumour rejection.9–11 This evidence suggests that, despite their small population size, NKT cells have potent effects on immune responses, and they facilitate different outcomes in different contexts. These properties are probably in large part a result of the ability of NKT cells to influence the functions of critical antigen-presenting cell (APC) types.

GRP-78 is a glucose-regulated protein belonging to the HSP-70 family, which is mainly present in the endoplasmic reticulum where it mediates several cellular processes as a chaperon, including protein folding, degradation of misfolded proteins, regulation of calcium homeostatis and sensing the endoplasmic reticulum stress.[32, 37-41] Recent studies indicate that a fraction of GRP-78 is also translocated to the cell surface in many cell types,[41] wherein it acts as the receptor mediating penetration and damage of endothelial cells by Mucorales, leading to the observed angioinvasion.[32] Mice with diabetic ketoacidosis

have an increased expression of GRP-78 in sinus, lungs JQ1 concentration and brain, and anti-GRP-78 serum can protect such mice from mucormycosis, indicating a plausible role of GRP-78 overexpression in susceptibility of diabetics

to this disease.[32, 39] It is generally believed that distinct clinical presentations of mucormycosis are associated with specific underlying risk factors, with ROC, pulmonary, gastrointestinal and cutaneous types occur in patients with diabetes, haematological malignancies or neutropaenia, severe malnutrition, and trauma or burns respectively.[1, 4-7] However, uncontrolled diabetes has been found as the major factor in all types of mucormycosis in India except the isolated renal form, although ROC manifestation remains the most common clinical type and is significantly associated with uncontrolled diabetes.[1, 4-7, HSP90 20, 21] As the Alpelisib majority of Indian patients have diabetes and metabolic acidosis as the major risk factors, the principal management modalities in such cases include a control of hyperglycaemia and prompt reversal of ketoacidosis, along with surgical debridement and amphotericin B therapy.[3] It is hypothesised that a decrease in diabetes-associated mucormycosis in USA in recent years may be attributed to an increased use of statins

in diabetic patients and the inhibitory action of statins against mucoralean agents.[42] Although statins are regularly prescribed in Indian patients with diabetes, no fall in the number of diabetes-associated mucormycosis cases has been reported from this country.[3] Therefore, a detailed study is required for assessing the role of statins against mucormycosis. Among the different clinical types of mucormycosis, cutaneous and rhino-cerebral types have a better survival rate due to possibility of an early diagnosis. Though majority of the Indian patients have rhino-cerebral presentation, the mortality rate of mucormycosis remains high (nearly 50%) in India.[4] This is largely due to a delay in seeking medical attention, diagnosis and therapy.[3] Apart from the common clinical types, isolated renal mucormycosis in apparently healthy hosts is being reported as a new clinical entity in India.[4-6, 43] Although the kidney is involved in nearly 22% cases of disseminated mucormycosis,[44] isolated renal mucormycosis is described rarely in literature.

On the other hand, defects in CD4+ Regulatory T cell (Treg) numbers and/or function contribute to T1D aetiology in NOD mice and in humans. In this work, we formally tested whether the protective role of the bacterial product lipopolysaccharide (LPS) on diabetes incidence results from enhanced Treg activity. We first report that weekly administration of LPS selleck chemicals llc to young prediabetic NOD mice, presenting or not insulitis at the time of treatment, afforded full protection from diabetes. Taking advantage from the high but incomplete penetrance of diabetes in NOD mice raised in specific pathogen free (SPF) conditions we compared untreated disease-free old animals with gender- and age-matched LPS-treated mice. Histological

and flow cytometry analysis indicated that LPS treatment did not prevent islet infiltration or priming of diabetogenic T cells but increased Foxp3+ and CD103+ Treg frequency and numbers. By performing adoptive transfer experiments into alymphoid NOD/SCID recipients, we further demonstrated that CD25+ cells from LPS-treated NOD mice, but not from naturally protected animals, maintained diabetogenic cells at check. Our study suggests that T cell regulation represents a cellular mechanism to explain the ‘hygiene hypothesis’ and reinforces the notion that immune activity consolidates dominant tolerance. The non-obese diabetic (NOD) mouse develops spontaneous autoimmune diabetes that closely resembles the human type

I diabetes (T1D) pathology. Beta cell destruction in NOD mice is T cell dependent and leads to impaired insulin production and consequently NVP-LDE225 order diabetes. Pancreatic islet inflammation is initiated around 3 weeks of age with infiltration by DC and macrophages, followed by the recruitment of lymphocytes. Despite extensive infiltration of the pancreatic islets, disease remains clinically silent for about another 12 weeks. GPX6 The observation that insulitis precedes diabetes by many weeks suggests that dominant regulatory mechanisms control disease progression. Several cell subsets were implicated in diabetes regulation, among which NK T and CD4+

Regulatory T cells (Treg) are the best studied [1]. NOD mice have lower number of Treg as compared with non-autoimmune mouse strains [2, 3]. Moreover, Treg in NOD animals undergo progressive loss of function with age [4–7]. In addition, analysis of T1D patients revealed decreased number [8] or functionally deficient Treg [9], when compared with healthy individuals. Hence, Treg alterations appear to take part of the aetiology of T1D in mice and in humans. Evidence that Treg are directly involved in limiting diabetes progression in mice, rats and humans is solid. Foxp3-deficient NOD mice exhibit increased incidence and earlier onset of diabetes as compared to WT NOD mice [10]. Moreover, monoclonal antibody (mAb)-mediated IL-2 neutralization, a protocol that decreases Treg numbers, precipitates diabetes in NOD mice [11] while IL-2 treatment prevents disease [12].

CD8− T cells (representing mainly T helper cells) were also analysed, although they were not the main focus of this work. The frequency of cells expressing a certain marker was calculated in relation to the number of cells in the relevant subset. Unstimulated samples were used as negative controls. spss 18.0 software was used for statistical analysis and P-values were corrected for multiple testing (Bonferroni-correction). For the purpose of this study heart and heart–lung recipients were generally treated as one group (transplant patients). This study was focused on CD8+ T cells but pp65-specific CD8− T cells were also explored. However, IE-1-specific CD8− T cells

were detected infrequently and the numbers LEE011 nmr were small, so this subset was not analysed further.12 The frequencies of inducible pp65-specific or IE1-specific CD8+ T cells or pp65-specific CD8− T cells were subject to large inter-individual variation. A trend towards smaller frequencies of IFN-γ-producing, TNF-α-producing or IL-2-producing IE1-specific CD8+ T cells in transplant patients was observed, but this was not true for pp65-specific CD8+ or CD8− T-cell responses. None of the observed differences was statistically significant (Fig. 1a). No difference was observed between patients who Talazoparib in vivo had received a CMV+

or a CMV– graft (not shown). Interferon-γ is a frequently used read-out for T-cell activation in the transplant setting; the median frequencies of CD8+ and CD8− T cells exhibiting ‘at least one marker’/IFN-γ-positive cells in % of the reference subset (either all CD8+ or CD8− T cells) were as follows, CD8+/pp65: transplant group 1·05/0·25, control 0·35/0·26; CD8+/IE-1: transplant group 0·58/0·14, control 0·70/0·52; CD8−/pp65: transplant group 0·34/0·14, control 0·43/0·18. Of interest, the differences in frequency between degranulating and triclocarban IFN-γ-producing cells were significant in transplant recipients

but not in controls (Fig. 1a). The same was true for the frequencies of degranulating compared with TNF-α-producing or IL-2-producing cells. With respect to pp65-specific CD8+ T cells all the same differences were also significant in heart recipients analysed separately. The lung recipients were a smaller group and not all of the same differences (though suggested by the data) were significant, in particular the differences with respect to pp65-specific CD8− T cells did not reach statistical significance (not shown). Of note, frequencies of IFN-γ+ T cells were significantly higher than IL-2+ T cells within the CD8+ subset of transplant patients for both antigens tested (P = 0·0006 for pp65 and P = 0·005 for IE1). Differences for the pp65 CD8− T cells were non-significant (P = 0·144). In summary, the data clearly demonstrated that degranulation of CD8+ T cells was the dominant function found under immunosuppression.

Because the early events occur within skin, this disease potentially offered a new human model whereby skin biopsies could allow direct study of the kinetics of the CD1 induction process in vivo or ex vivo 25, 26.

Here, we report that natural learn more and experimental B. burgdorferi infection upregulates cell surface expression of CD1a, CD1b and CD1c in the dermis of human skin. Although CD1d and NKT cells are thought to act at the earliest stages of the innate response, we found that the process of group 1 CD1 induction requires antecedent signaling through TLR-2 and a days long series of events whereby the cell-to-cell spread of cytokines leads to CD1 appearance on maturing DCs. Cilomilast These studies support a role for CD1 in host response in human Lyme disease and demonstrate a previously unknown pathway whereby IL-1β cleavage leads to selective induction of group 1 CD1 proteins after infection. Mechanistic studies of group 1 CD1 induction have been carried out using dispersed blood monocytes 12, 13, 19, highlighting the need for studies of infected human tissues. To determine whether group 1 CD1 proteins are induced within skin during natural B. burgdorferi infection, we first studied frozen sections of EM skin lesions from ten patients

with Lyme disease. The diagnosis of Lyme disease was confirmed by culture or serology, or in most instances, by both methods (Table 1). In addition to culture-positivity, three patients had evidence of spirochetes in the blood and >6 symptoms, including fever, headache, stiff neck, arthralgias, myalgias and fatigue; and two had multiple EM skin lesions. Eight patients were infected with B. burgdorferi OspC type A or K strains, the two most common B. burgdorferi genotypes 27, 28. Hoechst from dye staining viewed at low power showed nuclei clustering in rete patterns that corresponded to the dermal–epidermal junction (Fig. 1A), as confirmed in serial sections stained with hematoxylin and eosin (not shown). In two color immunohistochemistry

samples stained with anti-CD1a, many large cells were seen in the epidermis, likely representing Langerhans cells (LC), a DC subtype that constitutively expresses CD1a (Fig. 1A). In contrast, CD1b and CD1c in normal skin were consistently seen at low levels on about 1% of dermal cells (Fig. 1B and data not shown). For two patients (Table 1 – A and J), CD1b and CD1c could be detected with bright staining on many (∼5%) large cells in the dermis (Table 1, Fig. 1A). One of these two patients (A) had severe infection, with a positive PCR test for B. burgdorferi DNA in blood, >6 symptoms, and multiple EM lesions. Both patients (A and J) were infected with the OspC type A genotype, a particularly virulent B. burgdorferi subtype that grows to high numbers in EM lesions 27, 28.

13 Intriguingly, we found that treatment of BL cells MK-2206 cost with proteasome inhibitors partially restores their capacity to present the EBNA1 epitope, thereby suggesting that proteasomes from BL cells, although less active against prototype substrate peptides, which only partially indicate the in vivo proteasomal activities, degrade the HPV epitope during the processing of EBNA1. It

remains to be elucidated whether other EBNA1-derived CTL epitopes may be more efficiently generated and presented after partial inhibition of proteasomes or whether this effect is restricted to the HPV epitope. In conclusion, our study, together with previous reports, strongly supports the idea Selleck Small molecule library that EBNA1-specific CTLs might be exploited therapeutically to target EBV-positive malignancies in combination with chemotherapy and protocols designed to restore antigen-presenting capacity in the tumour. In this context, it has been recently demonstrated that tubacin, a molecule that inhibits histone deacetylase 6, demonstrates a fairly selective capacity

to induce apoptosis in BL cells, but not in LCLs.37 Furthermore, the combination of tubacin with a proteasome inhibitor induced efficient killing of BL cells,37 which are known to be resistant to proteasome inhibitor-induced apoptosis.21,38 These findings, together with those reported in this study, suggest that the use of proteasome inhibitors, alone or in combination with other drugs such as tubacin, may represent a strategy Isotretinoin for the treatment of EBNA1-carrying

tumours, because proteasome inhibitors, in addition to their effect as pro-apoptotic drugs, may also increase the immunogenicity of EBNA1, thereby resulting in the efficient elimination of EBNA1-positive malignancies. This work was supported by grants from the University of Ferrara and Fondazione Cassa di Risparmio di Ferrara. We are grateful to A. Forster for editorial assistance and to Dr A. Balboni for HLA typing. The authors have no financial conflicts of interest. Table S1. MHC class I expression in lymphoblastoid cell line and in Burkitt’s lymphoma cells. “
“EAE, an animal model for multiple sclerosis, is a Th17- and Th1-cell-mediated auto-immune disease, but the mechanisms leading to priming of encephalitogenicTcells in autoimmune neuroinflammation are poorly understood. To investigate the role of dendritic cells (DCs) in the initiation of autoimmuneTh17- andTh1-cell responses andEAE, we used mice transgenic for a simian diphtheria toxin receptor (DTR) expressed under the control of the murineCD11c promoter (CD11c-DTRmice onC57BL/6 background).EAEwas induced by immunization with myelin oligodendrocyte glycoprotein (MOG) protein in CFA.

Skin grafts are not suitable when deep structures are exposed. Local flaps are not available, particularly for defects of the toes. Free flaps are spared for larger defects. Medial plantar flap has been widely used for plantar defects, especially weight-bearing JQ1 mw surface of the heel. Distally based retrograde-flow design of this flap allows

the transfer of the pedicled flap distally and provides coverage of soft tissue over the metatarsal heads. In this report, we further modified the retrograde-flow medial plantar island flap to extend its use for distal dorsal forefoot defects. The technique and outcomes of two patients are presented. © 2010 Wiley-Liss, Inc. Microsurgery, 2010. “
“Background: An anterolateral thigh (ALT) flap has gradually become the workhorse flap of reconstructions at different anatomical locations because of its reliability and versatility. In this study, we introduced the concepts: one is the ALT flap harvest from a lateral approach and the other is the reconstruction of extensive head and neck defects with a single ALT donor site. Methods:

A lateral approach ALT flap was harvested in 13 patients who had buccal cancer and/or tumors of the lower lip combined with buccal trismus. Three types of ALT flaps (type I: two skin paddles, one pedicle; type II: two skin paddles, two pedicles; type III: one skin paddle, one pedicle) were used in one-stage reconstructions of these extensive head and neck defects. Results: In our series, there were four type I, five type II, and four type III flaps. All flaps survived and no major postoperative complication occurred. Four of the 13 donor sites were repaired with a split-thickness skin graft harvested from mTOR inhibitor the contralateral thigh. The immediate interincisor distance increase was 21.4 and 16.5 mm at 1-year follow-up. Celastrol Conclusions: Different types of ALT flap from a single donor site can be designed by means of a lateral approach; and the satisfactory results of reconstruction for extensive head and neck defects following the tumor resection and trismus release can be achieved. © 2012 Wiley Periodicals,

Inc. Microsurgery, 2012. “
“This study aimed at assessing the functional and electrophysiological recovery after vein wrapping of primary repaired ulnar nerves From January 2010 till December 2012, 23 patients (diagnosed with distal ulnar nerve injury) were prospectively studied where they were divided into two groups; group one (11 patients) and group two (12 patients). The injury was sharp in all cases but for one. The first group was managed by primary epineurorraphy. The second group was managed by primary epineurorraphy and autogenous vein wrapping. Final outcome was based on sensory recovery, motor recovery, and the presence or absence of electrophysiological response Clinically, only one case in each group exhibited negative Tinel’s sign. The second group achieved statistically significant superiority regarding motor recovery (P = 0.018), sensory recovery (P = 0.

For some comparative studies, similar cultures

were performed using unpulsed or C. neoformans-pulsed Mφ as APC. Furthermore, the production of IFN-γ, TNF-α, IL-4, IL-13 and IL-10 by purified T cells was measured in supernatants of 96-hr cultures using anti-(rat IFN-γ), anti-(rat-TNF-α), anti-(rat-IL-4), anti-(rat-IL-13) and anti-(rat-IL-10) CytoSets (BioSource), as described above. For intracellular cytokine and surface-marker staining, C. neoformans-primed CD4+ and CD8+ T cells (1 × 106 cells) were co-cultured with unpulsed or C. neoformans-pulsed eosinophils (2 × 105 cells), or in medium alone, for 4 days. Then, T cells were stimulated with phorbol 12-myristate 13-acetate (PMA; 50 ng per 2 × 106 this website cells), ionomycin (500 ng per 1 × 106 cells) and brefeldin A (5 ng/1 × 106 cells) for 3 hr at 37° under a 5% CO2 humidified atmosphere. For cell-surface staining, cells were incubated for 30 min at 4° in the dark with FITC-conjugated mouse mAb specific to rat CD4 (0·5 mg per 106 cells) or CD8 (0·5 mg per 106 cells). Dactolisib The cells were then washed twice (30 min each wash, at room temperature) with PBS containing 3% FCS and then fixed overnight at 4° in PBS containing 1% paraformaldehyde. Before intracellular cytokine staining, the cells were washed with PBS containing 0·5% saponin. Cells

in this buffer were incubated with phycoerythrin (PE)-conjugated mouse anti-(rat IFN-γ) (0·125–0·5 μg per 106 cells) and anti-(rat IL-4) (0·1–0·5 μg per 106 cells), or appropriate controls (corresponding to IgG-negative isotypes) in the dark for 30 min at room temperature. Etomidate The cells were washed twice with PBS containing 0·5% saponin and finally resuspended in 0·2 ml of flow wash.29 The immunofluorescently stained cells were analyzed

using a Becton Dickinson FACS Canto II flow cytometer (San José, CA). The percentage of double-positive labelled cells was determined using dot-plot graphs. Data were expressed as means + standard errors of the mean (SEM) and analyzed statistically using the Student’s t-test. Statistical significance was taken to be a P-value of < 0·05. All experiments were repeated and equivalent results were obtained. First, we evaluated the ability of eosinophils to phagocytose live yeasts of C. neoformans. Purified eosinophils were exposed to yeasts of C. neoformans that were either opsonized with the mAb 3C2 which binds specifically to C. neoformans glucuronoxylomannan, or non-opsonized, at a ratio of 1:1, in the presence or absence of GM-CSF (5 ng/ml) for 24 hr. Eosinophils incubated with opsonized C. neoformans, non-opsonized C. neoformans or medium alone, showed more than 85% viability, as determined using the Trypan Blue dye-exclusion test, and < 10% apoptosis when tested by propidium iodide staining and flow cytometry (data not shown).

Expression and purification of recombinant proteins was essentially the same as previously described (10, 12). Briefly, E. coli BL21 (DE3) cells harboring plasmid pET28a-S450–650, pET28a-CRT, or pET28a-S450–650/CRT were cultured in 1L 2YT medium containing kanamycin (30 μg/mL) at 37 °C. When the cell density had reached 0.8–1.0 (optical density 600), IPTG (Sigma-Aldrich, St Louis, MO, USA) was added to a final concentration of 0.1 mM, and the bacteria cultured for a further 3.5 hr at 37 °C. The culture was then harvested

by centrifugation and the cell pellet suspended in 40 mL binding buffer (500 mM NaCl, 20 mM Tris-HCl, 5 mM imidazole, pH 7.9). After sonication (4 s pulse, 4 s pause, 200 W 50 times), the lysed cells were centrifuged at 5000 g for 15 min at 4 °C. The supernatant was incubated with 2

mL Ni sepharose (GE Healthcare, Uppsala, Sweden) at 4 selleckchem °C for 1 hr. The sepharose was poured into a column and washed with 100 mL wash buffer (500 mM NaCl, 20 mM Tris-HCl, 20 mM imidazole, pH 7.9) and then the recombinant protein eluted with elute buffer (500 mM NaCl, 20 mM Tris-HCl, 500 mM imidazole, pH 7.9). The final products were dialyzed with PBS (pH 7.2) and stored at −20°C before use. S450–650-based ELISAs were performed according to the protocol previously described (8, 9). Briefly, ELISA plates were coated at 4 °C overnight with 2 μg/mL rS450–650 in carbonate buffer (pH 9.6). The wells selleck products were then incubated with 2% BSA in PBS for 2 hr at 37 °C, and then washed five times with PBST. Serum samples from immunized mice were diluted in dilution buffer (0.1% BSA in PBS). 100 μL of each dilution was added to each well and the plates incubated for 90 min at 37 °C. After washes with PBST, the Protein kinase N1 plates were incubated with 100 μL HRP-labeled goat anti-mouse IgG, IgG1 or IgG2a antibody (Southern Biotech, Birmingham, AL, USA) 1/4000 diluted in dilution buffer for 1 hr at 37 °C. OPD substrate (100 μL /well) was added after five washes with PBS-T and incubated at room temperature. 50 μL of 2M H2SO4 solution was

added to each well to stop the reaction, and the optical density was immediately read at 492 nm. Bone marrow was flushed out of the femora and tibiae of BALB/c mice and incubated at a starting concentration of 5 × 106 cells/mL in R10 medium in 6-well flat bottomed plates (Falcon, Oxnard, CA, USA) at 37 °C, 5% CO2 for 3 hr. Non-adherent cells were removed before recombinant mouse GM-CSF (rmGM-CSF, PeproTech EC, London, UK) was added to the culture (20 ng/mL). On day 3, half of the medium was replaced with fresh medium containing rmGM-CSF. On day 5, adherent cells were harvested as bone-marrow-derived immature DCs and examined microscopically and also by flow cytometry for expression of CD11c.

After 120 hrs, the mortality rate in WSSV-injected F. indicus experimental groups (5 and 35 g/L) was significantly higher than for F. indicus exposed to 25 and

15 g/L salinities. During the experimental period (0–120 hrs), biochemical variables, namely total protein, carbohydrate, and lipid concentrations, were measured in hemolymph of both experimental and control groups. Acute salinity changes induced an increase in protein variations across the tested salinity ranges in shrimp. After 24 hrs, THC and PO activity decreased significantly whereas RB, alkaline phosphatase and acid phosphatase activities increased in shrimps kept at the lower salinities of 5, 15 and 35 g/L. Concomitant with the rapid emergence of shrimp culture industries, effective disease management strategies Epigenetics Compound Library have become necessary. WSSV is a lethal

viral disease that affects cultured and captured Autophagy Compound Library chemical structure commercially important shrimp species and many other crustaceans [1]. In farmed shrimp, this virus reportedly causes 100% cumulative mortality in 2–10 days [1-4]. WSSV is an enveloped, ellipsoid, large (∼300 kb), double stranded DNA virus. In the infected tiger shrimp Penaeus monodon, common signs of the disease include appearance of white spots on the carapace, reddish discoloration around soft tissues, anorexia, lethargy and swelling Cobimetinib datasheet of branchiostegites [2]. Although WSSV has been formally recognized since 1992, the International Committee on the Taxonomy of Viruses has designated this virus as a new genus, Whispovirus, family Nimaviridae [5]. Disease is the end result of complex interactions between host, pathogen and environment. In this context, water salinity is considered one of the most important environmental factors for shrimp because it influences metabolism, oxygen consumption, feeding rate, growth, molting, survival and

tolerance to toxic metabolites [6]. Hemocytes counts, which correlate with prophenoloxidase (proPO), respiratory burst, SOD, and phagocytic activity have been used as indices of immune capability in penaeid shrimps [7]. Hemolymph metabolic variables such as proteins, glucose, cholesterol, triacylglycerol, have been found to vary in response to captivity stress, temperature alterations, depleted dissolved oxygen and high ambient ammonia [8]. Biochemical variables in hemolymph have also been identified as indicators of stress related to onset of shrimp disease. In the last 10 years, substantial progress has been made in quantifying WSSV in infected animals. Owing to the unavailability of immortal cell lines to determine viral load of viable virus, quantitative PCR has been the main method used for quantification. Dhar et al.