Dimensional Crossover of Weak Localization in a Magnetic Field

We study the dimensional crossover of weak localization in strongly anisotropic systems. This crossover from three-dimensional behavior to an effective lower dimensional system is triggered by increasing temperature if the phase coherence length gets shorter than the lattice spacing $a$. A similar effect occurs in a magnetic field if the magnetic length $L_m$ becomes shorter than $a(D_{||}/D_\perp)^\gamma$, where \D_{||}/D_\perp is the ratio of the diffusion coefficients parallel and perpendicular to the planes or chains. $\gamma$ depends on the direction of the magnetic field, e.g. $\gamma=1/4$ or 1/2 for a magnetic field parallel or perpendicular to the planes in a quasi two-dimensional system. We show that even in the limit of large magnetic field, weak localization is not fully suppressed in a lattice system. Experimental implications are discussed in detail.Comment: RevTeX, 11 pages, 4 figures; three references added and discusse

Regulation of inflammation in Japanese encephalitis

Uncontrolled inflammatory response of the central nervous system is a hallmark of severe Japanese encephalitis (JE). Although inflammation is necessary to mount an efficient immune response against virus infections, exacerbated inflammatory response is often detrimental. In this context, cells of the monocytic lineage appear to be important forces driving JE pathogenesis

Cellular immune responses to live attenuated Japanese Encephalitis (JE) vaccine SA14-14-2 in adults in a JE/dengue co-endemic area.

Background Japanese encephalitis (JE) virus (JEV) causes severe epidemic encephalitis across Asia, for which the live attenuated vaccine SA14-14-2 is being used increasingly. JEV is a flavivirus, and is closely related to dengue virus (DENV), which is co-endemic in many parts of Asia, with clinically relevant interactions. There is no information on the human T cell response to SA14-14-2, or whether responses to SA14-14-2 cross-react with DENV. We used live attenuated JE vaccine SA14-14-2 as a model for studying T cell responses to JEV infection in adults, and to determine whether these T cell responses are cross-reactive with DENV, and other flaviviruses. Methods We conducted a single arm, open label clinical trial (registration: clinicaltrials.gov NCT01656200) to study T cell responses to SA14-14-2 in adults in South India, an area endemic for JE and dengue. Results Ten out of 16 (62.5%) participants seroconverted to JEV SA14-14-2, and geometric mean neutralising antibody (NAb) titre was 18.5. Proliferation responses were commonly present before vaccination in the absence of NAb, indicating a likely high degree of previous flavivirus exposure. Thirteen of 15 (87%) participants made T cell interferon-gamma (IFNγ) responses against JEV proteins. In four subjects tested, at least some T cell epitopes mapped cross-reacted with DENV and other flaviviruses. Conclusions JEV SA14-14-2 was more immunogenic for T cell IFNγ than for NAb in adults in this JE/DENV co-endemic area. The proliferation positive, NAb negative combination may represent a new marker of long term immunity/exposure to JE. T cell responses can cross-react between JE vaccine and DENV in a co-endemic area, illustrating a need for greater knowledge on such responses to inform the development of next-generation vaccines effective against both diseases.</p

Cellular Immune Responses to Live Attenuated Japanese Encephalitis (JE) Vaccine SA14-14-2 in Adults in a JE/dengue Co- Endemic Area

Background: Japanese encephalitis (JE) virus (JEV) causes severe epidemic encephalitis across Asia, for which the live attenuated vaccine SA14-14-2 is being used increasingly. JEV is a flavivirus, and is closely related to dengue virus (DENV), which is co-endemic in many parts of Asia, with clinically relevant interactions. There is no information on the human T cell response to SA14-14-2, or whether responses to SA14-14-2 cross-react with DENV. We used live attenuated JE vaccine SA14-14-2 as a model for studying T cell responses to JEV infection in adults, and to determine whether these T cell responses are cross-reactive with DENV, and other flaviviruses. Methods: We conducted a single arm, open label clinical trial (registration: clinicaltrials.gov NCT01656200) to study T cell responses to SA14-14-2 in adults in South India, an area endemic for JE and dengue. Results: Ten out of 16 (62.5%) participants seroconverted to JEV SA14-14-2, and geometric mean neutralising antibody (NAb) titre was 18.5. Proliferation responses were commonly present before vaccination in the absence of NAb, indicating a likely high degree of previous flavivirus exposure. Thirteen of 15 (87%) participants made T cell interferon-gamma (IFNγ) responses against JEV proteins. In four subjects tested, at least some T cell epitopes mapped cross-reacted with DENV and other flaviviruses. Conclusions: JEV SA14-14-2 was more immunogenic for T cell IFNγ than for NAb in adults in this JE/DENV co-endemic area. The proliferation positive, NAb negative combination may represent a new marker of long term immunity/exposure to JE. T cell responses can cross-react between JE vaccine and DENV in a co-endemic area, illustrating a need for greater knowledge on such responses to inform the development of next-generation vaccines effective against both diseases

Seroepidemiology of hepatitis A in voluntary blood donors from Pune, western India (2002 and 2004–2005)

Recently, a changing pattern of hepatitis A epidemiology has been reported in the Indian population indicating a rise in the rate of hepatitis A infection among adults. The study's objective was to assess anti-HAV prevalence in voluntary blood donors from middle and high socioeconomic strata. Serum samples collected from voluntary blood donors from Pune city and its suburbs in the years 2002 and 2004–2005 were tested for anti-HAV IgG antibodies. Serum samples collected during 2004–2005 were examined for anti-HAV IgM antibodies. Positive samples were tested for HAV-RNA. Agewise anti-HAV positivity was significantly low in adults aged 18–25 years (90·4%) compared to those aged >25 years (97·4%) (P<0·01). A decline in anti-HAV prevalence was significant in 2004–2005 compared to that in 2002 (96·5% vs. 92·1%) (P<0·01). Overall, in both adult age groups, the proportion of anti-HAV positivity was remarkably low in the high socioeconomic group (HSG) (88·96%) compared to that of the middle socioeconomic group (MSG) (95·86%) (P<0·01). Anti-HAV IgM positivity was not significant (~1%), however, presence of HAV-RNA in one of the samples indicated the possibility of horizontal transmission of HAV. Increase in seronegativity to HAV in HSG implicates a rise in the susceptible pool and indicates the need for vaccination against hepatitis A

Antibody and cellular responses to JE vaccine SA14-14-2.

<p>(A) Neutralisation of JEV SA14-14-2 by sera from vaccinated participants at 4 weeks, 8 weeks and 4–6 months after vaccination. Data are the logarithm of the geometric mean of 1/plaque reduction neutralisation titre 50% (PRNT₅₀) ± 95% confidence interval (CI). Filled circles = responders, open circles = non-responders. The number of participants with data at each time point are indicated. (B) IFNγ-ELISpot responses to a peptide library of JEV SA14-14-2 after vaccination. Data are the geometric mean of the sum of spot forming cells (SFC)/10⁶ PBMC for all responding pools (per participant) after subtraction of background wells at each time point ± 95% CI. Non-responding pools were not included. The number of participants is indicated as in (A). Responses were significantly increased over baseline at weeks 1, 2 and 4 (Wilcoxon signed rank test). (C) Proliferation responses in 13 JE vaccinated individuals. Data represent the average % responding cells (CFSE^lo/CD38^hi) measured by flow cytometry across all peptide pools tested in the CD4⁺ (filled circles) or CD8⁺ (open circles) gate. Data points are the median and error bars depict the interquartile range (IQR). The number of participants is indicated as in (A).</p

Targeting of IFNγ responses to JEV SA14-14-2.

<p>(A) Sum of all responding pools (IFNγ SFC/10⁶ PBMC by ELISpot) against the number of responding pools at the time of maximum ELISpot response per participant in the study. (B) Number of participants responding to each protein of JEV in ELISpot assays, normalised to the protein size as responses per 100 amino acids. (C & D) Peptide pools were deconvoluted by <i>ex-vivo</i> ELISpot, or in ICS assays using T cell lines expanded to peptide pools. Location of epitopes mapped to individual peptides (C) and to “mini-pools” spanning regions 46–90 amino acids in size (D). The Y axes represent the number of responses identified (one of the six “mini-pool” regions identified was recognised by two participants). Subsets were determined by flow cytometry. CD4⁺ responses: green bars; CD8⁺ responses: blue bars. The single grey bar in (C) depicts a response identified by ELISpot where the subset was not determined.</p