Latency (engineering)

About: Latency (engineering) is a research topic. Over the lifetime, 7278 publications have been published within this topic receiving 115409 citations. The topic is also known as: lag.

Contention-Based Access for Ultra-Reliable Low Latency Uplink Transmissions

Abstract: We consider a sporadic ultra-reliable and low latency communications in the uplink 5G cellular systems. Reliable low latency access for randomly emerging packet transmission cannot be guaranteed in current wireless systems. To achieve the goal of low latency and high reliability simultaneously, we propose a contention-based transmission scheme aimed at users with small payloads. We seek to reduce collision probability by considering multiple transmissions for the same packet for reliable reception. We find the optimal number of consecutive multiple transmissions that reduces collisions and achieves target reliability within the latency window. Performance is analyzed with a frame structure planned for 5G cellular systems. Results are compared with default multi-channel slotted ALOHA access scheme.

A Novel Low-Latency V2V Resource Allocation Scheme Based on Cellular V2X Communications

Abstract: In vehicular ad hoc networks (VANETs), cellular vehicle-to-everything (C-V2X) is an emerging technology for communications between vehicle-to-infrastructure, vehicle-to-pedestrian, and vehicle-to-network which improves traffic efficiency, road safety, and the availability of infotainment services. Herein, a novel V2V-enabled resource allocation scheme based on C-V2X technology is proposed to improve the reliability and latency of VANETs. The key idea is that V2V communications based on cellular-V2X technology among vehicles remove the contention latency and can assist for longer distance communications. Particularly, we propose a hybrid architecture, where the V2V links are controlled by the cellular eNodeB in the overlay scheme. In this scheme, every vehicle periodically checks its packet lifetime and requests the cellular eNodeB to determine V2V links. The optimum resource allocation problem at the cellular eNodeB is to choose optimum receiver vehicles to determine V2V links and allocate suitable channels to minimize the total latency. This problem is equivalent to the maximum weighted independent set problem (MWIS-AW) with associated weights, which is NP-hard. In order to compute the weights, an analytical approach is developed to model the expected latency and packet delivery ratio. Moreover, a greedy cellular-based V2V link selection algorithm is proposed to solve MWIS-AW problem and develop a theoretical performance lower bound. Simulation results show that the proposed scheme significantly outperforms the existing schemes in terms of latency, throughput, and packet delivery ratio.

Cellular and molecular mechanisms involved in the establishment of HIV-1 latency

Abstract: Latently infected cells represent the major barrier to either a sterilizing or a functional HIV-1 cure. Multiple approaches to reactivation and depletion of the latent reservoir have been attempted clinically, but full depletion of this compartment remains a long-term goal. Compared to the mechanisms involved in the maintenance of HIV-1 latency and the pathways leading to viral reactivation, less is known about the establishment of latent infection. This review focuses on how HIV-1 latency is established at the cellular and molecular levels. We first discuss how latent infection can be established following infection of an activated CD4 T-cell that undergoes a transition to a resting memory state and also how direct infection of a resting CD4 T-cell can lead to latency. Various animal, primary cell, and cell line models also provide insights into this process and are discussed with respect to the routes of infection that result in latency. A number of molecular mechanisms that are active at both transcriptional and post-transcriptional levels have been associated with HIV-1 latency. Many, but not all of these, help to drive the establishment of latent infection, and we review the evidence in favor of or against each mechanism specifically with regard to the establishment of latency. We also discuss the role of immediate silent integration of viral DNA versus silencing of initially active infections. Finally, we discuss potential approaches aimed at limiting the establishment of latent infection.

Device Power Saving and Latency Optimization in LTE-A Networks Through DRX Configuration

Abstract: Discontinuous reception (DRX) saves battery power of user equipment (UE) usually at the expense of potential increase in latency in the Long Term Evolution (LTE) networks. Therefore, an optimization is needed to find the best tradeoff between latency and power saving. In this paper, we first develop an analytical model to estimate power saving achieved and latency incurred by DRX mechanism for active and background mobile traffic. A tradeoff scheme is then formulated to maintain a balance between these two performance parameters based on operator's preference for power saving and latency requirement of traffic. The analytical model is validated using system level simulation results obtained from OPNET Modeler. The results show that the proposed tradeoff scheme is efficient in keeping a balance between power saving and latency. The results also indicate that DRX short cycles are very effective in reducing latency for active traffic, while shorter inactivity timer is desirable for background traffic to enhance power saving. We also proposed a mechanism to switch DRX configuration based on traffic running at UE, using UE assistance procedure recently adopted by 3GPP in Release 11. DRX configuration switching increases the power saving significantly without any noticeable increase in latency of active traffic.

Herpes Simplex Virus Type 2 (HSV-2) Establishes Latent Infection in a Different Population of Ganglionic Neurons than HSV-1: Role of Latency-Associated Transcripts

Abstract: Herpes simplex virus type 1 (HSV-1) and HSV-2 cause very similar acute infections but differ in their abilities to reactivate from trigeminal and dorsal root ganglia. To investigate differences in patterns of viral infection, we colabeled murine sensory ganglia for evidence of HSV infection and for the sensory neuron marker A5 or KH10. During acute infection, 7 to 10% of HSV-1 or HSV-2 antigen-positive neurons were A5 positive and 13 to 16% were KH10 positive, suggesting that both viruses reach each type of neuron in a manner proportional to their representation in uninfected ganglia. In murine trigeminal ganglia harvested during HSV latency, 25% of HSV-1 latency-associated transcript (LAT)- and 4% of HSV-2 LAT-expressing neurons were A5 positive, while 12% of HSV-1 LAT- and 42% of HSV-2 LAT-expressing neurons were KH10 positive. A similar difference was observed in murine dorsal root ganglia. These differences could not be attributed to differences in LAT expression levels in A5- versus KH10-positive neurons. Thus, HSV-1 demonstrated a preference for the establishment of latency in A5-positive neurons, while HSV-2 demonstrated a preference for the establishment of latency in KH10-positive neurons. A chimeric HSV-2 mutant that expresses the HSV-1 LAT exhibited an HSV-1 phenotype, preferentially establishing latency in A5-positive neurons. These data imply that the HSV-1 and HSV-2 LAT regions influence the ability of virus to establish latency in different neuronal subtypes. That the same chimeric virus has a characteristic HSV-1 reactivation phenotype further suggests that LAT-influenced establishment of latency in specific neuronal subtypes could be an important part of the mechanism by which LAT influences viral reactivation phenotypes.