Zero Knowledge Protocols from Succinct Constraint Detection

We study the problem of constructing proof systems that achieve both soundness and zero knowledge unconditionally (without relying on intractability assumptions). Known techniques for this goal are primarily *combinatorial*, despite the fact that constructions of interactive proofs (IPs) and probabilistically checkable proofs (PCPs) heavily rely on *algebraic* techniques to achieve their properties. We present simple and natural modifications of well-known algebraic IP and PCP protocols that achieve unconditional (perfect) zero knowledge in recently introduced models, overcoming limitations of known techniques. 1. We modify the PCP of Ben-Sasson and Sudan [BS08] to obtain zero knowledge for NEXP in the model of Interactive Oracle Proofs [BCS16,RRR16], where the verifier, in each round, receives a PCP from the prover. 2. We modify the IP of Lund, Fortnow, Karloff, and Nisan [LFKN92] to obtain zero knowledge for #P in the model of Interactive PCPs [KR08], where the verifier first receives a PCP from the prover and then interacts with him. The simulators in our zero knowledge protocols rely on solving a problem that lies at the intersection of coding theory, linear algebra, and computational complexity, which we call the *succinct constraint detection* problem, and consists of detecting dual constraints with polynomial support size for codes of exponential block length. Our two results rely on solutions to this problem for fundamental classes of linear codes: * An algorithm to detect constraints for Reed--Muller codes of exponential length. This algorithm exploits the Raz--Shpilka [RS05] deterministic polynomial identity testing algorithm, and shows, to our knowledge, a first connection of algebraic complexity theory with zero knowledge. * An algorithm to detect constraints for PCPs of Proximity of Reed--Solomon codes [BS08] of exponential degree. This algorithm exploits the recursive structure of the PCPs of Proximity to show that small-support constraints are locally spanned by a small number of small-support constraints

Cytomegalovirus infection in pediatric rheumatic diseases: a review

Human cytomegalovirus (HCMV) is familiar to pediatric rheumatologists mainly as a cause of opportunistic disease in pharmacologically immune suppressed patients. However, HCMV also has a variety of immuno-modulatory effects, through which it may influence the course of rheumatic conditions. In this article we discuss the interplay between HCMV and the immune system, and review the clinical manifestations, diagnosis, and treatment of HCMV infection in children with rheumatic disease

Glucocortiocoid Treatment of MCMV Infected Newborn Mice Attenuates CNS Inflammation and Limits Deficits in Cerebellar Development

Infection of the developing fetus with human cytomegalovirus (HCMV) is a major cause of central nervous system disease in infants and children; however, mechanism(s) of disease associated with this intrauterine infection remain poorly understood. Utilizing a mouse model of HCMV infection of the developing CNS, we have shown that peripheral inoculation of newborn mice with murine CMV (MCMV) results in CNS infection and developmental abnormalities that recapitulate key features of the human infection. In this model, animals exhibit decreased granule neuron precursor cell (GNPC) proliferation and altered morphogenesis of the cerebellar cortex. Deficits in cerebellar cortical development are symmetric and global even though infection of the CNS results in a non-necrotizing encephalitis characterized by widely scattered foci of virus-infected cells with mononuclear cell infiltrates. These findings suggested that inflammation induced by MCMV infection could underlie deficits in CNS development. We investigated the contribution of host inflammatory responses to abnormal cerebellar development by modulating inflammatory responses in infected mice with glucocorticoids. Treatment of infected animals with glucocorticoids decreased activation of CNS mononuclear cells and expression of inflammatory cytokines (TNF-α, IFN-β and IFNγ) in the CNS while minimally impacting CNS virus replication. Glucocorticoid treatment also limited morphogenic abnormalities and normalized the expression of developmentally regulated genes within the cerebellum. Importantly, GNPC proliferation deficits were normalized in MCMV infected mice following glucocorticoid treatment. Our findings argue that host inflammatory responses to MCMV infection contribute to deficits in CNS development in MCMV infected mice and suggest that similar mechanisms of disease could be responsible for the abnormal CNS development in human infants infected in-utero with HCMV