Reservoirs for Human Immunodeficiency Virus

I received a very interesting letter to the editor from Dr. Hassan et al. regarding the potential role of monocytes and macrophages as a nonmemory T cell latent reservoir for human immunodeficiency virus (HIV). The letter, which is published in this issue of Viral Immunology, points out that the perinatally infected “Mississippi Baby” was able to suppress its HIV load after an initial round of antiviral therapy was discontinued. Interestingly, the baby's immune system was able to control the virus for 2 years in the absence of therapy until the virus finally rebounded. Since memory CD4⁺ T cells do not develop until after birth, the authors put forward a strong case that monocytes/macrophages may have been the crucial viral reservoir in this situation. This idea is important since characterization of viral replication and latency in these cell types will be critical for the development of new therapies and vaccines.

Two additional articles in the current issue of Viral Immunology address aspects of the innate immune response to viral infections. Askari et al. note that nucleotide-binding domain leucine repeats (NLRs) are required for the recognition of various microbial gene products and the subsequent activation of cytokine responses. The authors analyze the expression of NLRP1 and NLRC4 (components of inflammasomes) in chronically hepatitis B virus (HBV)-infected patients. Surprisingly, the data indicate that these genes are not induced in these patients, suggesting that they are not involved in the impaired immune response to HBV. A second article focuses on plasminogen activator inhibitor 1 (PAI-1). PAI-1 a protease inhibitor that inhibits fibrinolysis is reported to play a significant role in fibrosis occurrence and progression in inflammatory states in which fibrin is deposited in tissues. El Edel et al. have investigated PAI-1 polymorphisms in hepatitis C virus (HCV)-induced hepatocellular carcinoma, HCV-induced liver cirrhosis, and viral infection-free healthy control subjects. The authors document higher serum PAI-1 in HCV-induced hepatocellular carcinoma than viral infection-free controls, but interestingly, lower than HCV-induced liver cirrhosis patients. This was not genotype related. Further studies will be needed to clearly elucidate the underlying mechanism.

The remaining articles in this issue focus on the adaptive immune response. Assaf et al. have analyzed influenza vaccine coverage in 3,200 adult residents of Jordan from 2008 to 2012. The authors find that the coverage rates were low in Jordan than in other countries and recommend that influenza vaccine campaigns and on-going education in Jordan health schools to remove misconceptions and negative attitudes toward vaccination increase the coverage rate. Also on the vaccination front, Wang et al. note that the mucosal immune response plays a critical role in controlling porcine epidemic diarrhea virus (PEDV) infection in piglets. The authors have developed and tested a PEDV vaccine comprising a recombinant yeast expressing the PEDV S1 gene. Oral delivery of the vaccine to piglets induced a fecal IgA response that could be readily detected at 7 and 28 days postvaccination. Finally, Li and Ni have developed an epitope chimeric protein vaccine that is designed to break tolerance to HBV in infected individuals and induce protective immunity. The authors show the efficacy of the vaccine using HBV transgenic mice and note that antibodies induced by the vaccine have the ability to prevent HBV infection of human hepatocytes.

I would like to thank the authors for their excellent contributions to the Journal and all of the reviewers for their efforts to ensure the high quality of published articles.