Our goal was to describe the presence of HIV drug resistance among HIV-1-infected, antiretroviral (ARV) naïve children and adolescents in Latin America and to examine resistance in these children in relation to drug exposure in the mother. Genotyping was performed on plasma samples obtained at baseline from HIV-1-infected participants in a prospective cohort study in Brazil, Argentina, and Mexico (NISDI Pediatric Study). Of 713 HIV-infected children enrolled, 69 were ARV naïve and eligible for the analysis. At enrollment, mean age was 7.3 years; 81.2% were infected with HIV perinatally. Drug resistance mutations (DRMs) were detected in 6 (8.7%; 95% confidence interval 3.1–18.2%) ARV-naïve subjects; none of the mothers of these 6 received ARVs during their pregnancies and none of the children received ARV prophylaxis. Reverse transcriptase mutations K70R and K70E were detected in 3 and 2 subjects, respectively; protease mutation I50 V was detected in 1 subject. Three of the 6 children with DRMs initiated ARV therapy during followup, with a good response in 2. The overall rate of primary drug resistance in this pediatric HIV-infected population was low, and no subjects had more than 1 DRM. Mutations associated with resistance to nucleoside reverse transcriptase inhibitors were the most prevalent.

Luis E. Soto-Ramirez

Roberto Rodriguez-Diaz

D. Robert Harris

Rohan Hazra

HIV Drug Resistance-Associated Mutations in Antiretroviral Naïve HIV-1-Infected Latin American Children

Kaposi's sarcoma-associated herpesvirus (KSHV) is the aetiological agent of Kaposi's sarcoma (KS), the most frequently arising malignancy in individuals with untreated HIV/AIDS. There are several lines of evidence to indicate that Kaposi's sarcoma oncogenesis is associated with loss of T-cell-mediated control of KSHV-infected cells. KSHV can establish life-long asymptomatic infection in immune-competent individuals. However, when T-cell immune control declines, for example, through AIDS or treatment with immunosuppressive drugs, both the prevalence of KSHV infection and the incidence of KS in KSHV carriers dramatically increase. Moreover, a dramatic and spontaneous improvement in KS is frequently seen when immunity is restored, for example, through antiretroviral therapy or the cessation of iatrogenic drugs. In this paper we describe the current state of knowledge on the T-cell immune responses against KSHV.

Rebecca C. Robey

Salvinia Mletzko

Frances M. Gotch

The T-Cell Immune Response against Kaposi&#39;s Sarcoma-Associated Herpesvirus

Porcine reproductive and respiratory syndrome virus (PRRSV) is a major pathogen of swine worldwide and causes considerable economic loss. Identifying specific cell signaling or activation pathways that associate with variation in PRRSV replication and macrophage function may lead to identification of novel gene targets for the control of PRRSV infection. Serial Analysis of Gene Expression (SAGE) was used to create and survey the transcriptome of <i  >in vitro</i> mock-infected and PRRSV strain VR-2332-infected porcine alveolar macrophages (PAM) at 0, 6, 12, 16, and 24 hours after infection. The transcriptome data indicated changes in transcript abundance occurring in PRRSV-infected PAMs over time after infection with more than 590 unique tags with significantly altered transcript abundance levels identified (<svg     style="vertical-align:-0.1638pt;width:50.549999px;" id="M1" height="11.375" version="1.1" viewBox="0 0 50.549999 11.375" width="50.549999"  xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg">
	
		
			<g transform="matrix(.017,-0,0,-.017,.062,11.112)"><path id="x1D443" d="M619 482q0 -69 -40.5 -119t-96 -72.5t-118.5 -26.5h-44l-70 20l-31 -151q-14 -67 0.5 -83t89.5 -22l-5 -28h-287l8 28q65 7 81.5 22t29.5 83l79 398q12 56 0.5 70.5t-78.5 20.5l7 28h255q108 0 164 -43t56 -125zM524 478q0 141 -146 141q-25 0 -47 -8q-16 -6 -20.5 -13.5&#xA;t-10.5 -39.5l-43 -241q37 -13 83 -13q67 0 125.5 45t58.5 129z" /></g><g transform="matrix(.017,-0,0,-.017,15.582,11.112)"><path id="x3C" d="M512 -3l-437 233v51l437 233v-58l-378 -200v-2l378 -199v-58z" /></g><g transform="matrix(.017,-0,0,-.017,30.286,11.112)"><path id="x2E" d="M113 -12q-24 0 -39.5 16t-15.5 42q0 24 16 40.5t40 16.5t40 -16.5t16 -40.5q0 -26 -16 -42t-41 -16z" /></g><g transform="matrix(.017,-0,0,-.017,34.162,11.112)"><path id="x30" d="M241 635q53 0 94 -28.5t63.5 -76t33.5 -102.5t11 -116q0 -58 -11 -112.5t-34 -103.5t-63.5 -78.5t-94.5 -29.5t-95 28t-64.5 75t-34.5 102.5t-11 118.5q0 58 11.5 112.5t34.5 103t64.5 78t95.5 29.5zM238 602q-32 0 -55.5 -25t-35.5 -68t-17.5 -91t-5.5 -105&#xA;q0 -76 10 -138.5t37 -107.5t69 -45q32 0 55.5 25t35.5 68.5t17.5 91.5t5.5 105t-5.5 105.5t-18 92t-36 68t-56.5 24.5z" /></g><g transform="matrix(.017,-0,0,-.017,42.321,11.112)"><path id="x31" d="M384 0h-275v27q67 5 81.5 18.5t14.5 68.5v385q0 38 -7.5 47.5t-40.5 10.5l-48 2v24q85 15 178 52v-521q0 -55 14.5 -68.5t82.5 -18.5v-27z" /></g>

		
	
</svg>). Strikingly, innate immune genes (whose transcript abundances are typically altered in response to other pathogens or insults including IL-8, CCL4, and IL-1<i  >&#x3b2;</i>) showed no or very little change at any time point following infection.

Laura C. Miller

John D. Neill

Gregory P. Harhay

Kelly M. Lager

William W. Laegreid

Marcus E. Kehrli

In-Depth Global Analysis of Transcript Abundance Levels in Porcine Alveolar Macrophages Following Infection with Porcine Reproductive and Respiratory Syndrome Virus

APOBEC proteins appeared in the cellular battle against HIV-1 as part of intrinsic cellular immunity. The antiretroviral activity of some of these proteins is overtaken by the action of HIV-1 Viral Infectivity Factor (Vif) protein. Since the discovery of APOBEC3G (A3G) as an antiviral factor, many advances have been made to understand its mechanism of action in the cell and how Vif acts in order to counteract its activity. The mainstream concept is that Vif overcomes the innate antiviral activity of A3G by direct protein binding and promoting its degradation via the cellular ubiquitin/proteasomal pathway. Vif may also inhibit A3G through mechanisms independent of proteasomal degradation. Binding of Vif to A3G is essential for its degradation since disruption of this interaction is predicted to stimulate intracellular antiviral immunity. In this paper we will discuss the different binding partners between both proteins as one of the major challenges for the development of new antiviral drugs.

Iris Cadima-Couto

Joao Goncalves

Towards Inhibition of Vif-APOBEC3G Interaction: Which Protein to Target?

Dengue has been recognized as one of the most important vector-borne emerging infectious diseases globally. Though dengue normally causes a self-limiting infection, some patients may develop a life-threatening illness, dengue hemorrhagic fever (DHF)/dengue shock syndrome (DSS). The reason why DHF/DSS occurs in certain individuals is unclear.  Studies in the endemic regions suggest that the preexisting antibodies are a risk factor for DHF/DSS. Viremia and thrombocytopenia are the key clinical features of dengue virus infection in patients. The amounts of virus circulating in patients are highly correlated with severe dengue disease, DHF/DSS. Also, the disturbance, mainly a transient depression, of hematological cells is a critical clinical finding in acute dengue patients. However, the cells responsible for the dengue viremia are unresolved in spite of the intensive efforts been made. Dengue virus appears to replicate and proliferate in many adapted cell lines, but these in vitro properties are extremely difficult to be reproduced in primary cells or in vivo. This paper summarizes reports on the permissive cells in vitro and in vivo and suggests a hematological cell lineage for dengue virus infection in vivo, with the hope that a new focus will shed light on further understanding of the complexities of dengue disease.

Sansanee Noisakran

Nattawat Onlamoon

Pucharee Songprakhon

Hui-Mien Hsiao

Kulkanya Chokephaibulkit

Guey Chuen Perng

Cells in Dengue Virus Infection In Vivo

The RNA-dependent RNA-polymerase, <svg     style="vertical-align:-0.1638pt;width:36.737499px;" id="M1" height="16.9625" version="1.1" viewBox="0 0 36.737499 16.9625" width="36.737499"  xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg">
	
		
			<g transform="matrix(.017,-0,0,-.017,.062,16.7)"><path id="x33" d="M285 378v-2q65 -13 102 -54.5t37 -97.5q0 -57 -30.5 -104.5t-74 -75t-85.5 -42t-72 -14.5q-31 0 -59.5 11t-40.5 23q-19 18 -16 36q1 16 23 33q13 10 24 0q58 -51 124 -51q55 0 88 40t33 112q0 64 -39 96.5t-88 32.5q-29 0 -64 -11l-6 29q77 25 118 57.5t41 84.5&#xA;q0 45 -26.5 69.5t-68.5 24.5q-67 0 -120 -79l-20 20l43 63q51 56 127 56h1q66 0 107 -37t41 -95q0 -42 -31 -71q-22 -23 -68 -54z" /></g><g transform="matrix(.017,-0,0,-.017,8.222,16.7)"><path id="x44" d="M43 650h280q194 0 282 -85q85 -82 85 -215q0 -173 -123 -267q-107 -83 -297 -83h-236v27q65 5 79.5 19.5t14.5 77.5v402q0 45 -6 62.5t-21.5 24t-57.5 9.5v28zM213 547v-416q0 -55 24.5 -75t81.5 -20q133 0 203 86t70 214q0 80 -30 143t-88 97q-66 41 -170 41&#xA;q-62 0 -78 -13q-13 -9 -13 -57z" /></g>

			<g transform="matrix(.012,-0,0,-.012,20.712,8.537)"><path id="x70" d="M169 380l92 53q26 16 49 16q80 0 128.5 -56t48.5 -133q0 -108 -72.5 -180.5t-176.5 -91.5q-38 1 -69 18v-131q0 -57 13 -70t71 -18v-27h-236v27q49 5 61 17t12 61v452q0 48 -9.5 58.5t-56.5 16.5v24q66 11 145 43v-79zM169 346v-270q37 -39 94 -39q63 0 101.5 50&#xA;t38.5 134q0 78 -38.5 123t-95.5 45q-45 0 -100 -43z" /></g><g transform="matrix(.012,-0,0,-.012,27.055,8.537)"><path id="x6F" d="M257 449q92 0 154 -65t62 -158q0 -112 -67 -175t-150 -63q-98 0 -158.5 66.5t-60.5 154.5q0 59 21 106.5t54.5 75.5t71 43t73.5 15zM244 416q-48 0 -81 -47t-33 -128q0 -96 38 -158t99 -62q51 0 82 43.5t31 139.5q0 91 -36 151.5t-100 60.5z" /></g><g transform="matrix(.012,-0,0,-.012,33.052,8.537)"><path id="x6C" d="M238 0h-223v26q48 5 60 17t12 61v473q0 50 -10.5 60.5t-58.5 15.5v24q73 8 148 35v-608q0 -49 11.5 -61t60.5 -17v-26z" /></g>

		
	
</svg>, is an essential component in the picornavirus genome for the replication of single stranded RNA. However, transgenic expression of <svg     style="vertical-align:-0.1638pt;width:36.737499px;" id="M2" height="16.9625" version="1.1" viewBox="0 0 36.737499 16.9625" width="36.737499"  xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg">
	
		
			<g transform="matrix(.017,-0,0,-.017,.062,16.7)"><use xlink:href="#x33"/></g><g transform="matrix(.017,-0,0,-.017,8.222,16.7)"><use xlink:href="#x44"/></g>

			<g transform="matrix(.012,-0,0,-.012,20.712,8.537)"><use xlink:href="#x70"/></g><g transform="matrix(.012,-0,0,-.012,27.055,8.537)"><use xlink:href="#x6F"/></g><g transform="matrix(.012,-0,0,-.012,33.052,8.537)"><use xlink:href="#x6C"/></g>

		
	
</svg> in mice has antiviral effects. Here, we discuss the structure and function of <svg     style="vertical-align:-0.1638pt;width:36.737499px;" id="M3" height="16.9625" version="1.1" viewBox="0 0 36.737499 16.9625" width="36.737499"  xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg">
	
		
			<g transform="matrix(.017,-0,0,-.017,.062,16.7)"><use xlink:href="#x33"/></g><g transform="matrix(.017,-0,0,-.017,8.222,16.7)"><use xlink:href="#x44"/></g>

			<g transform="matrix(.012,-0,0,-.012,20.712,8.537)"><use xlink:href="#x70"/></g><g transform="matrix(.012,-0,0,-.012,27.055,8.537)"><use xlink:href="#x6F"/></g><g transform="matrix(.012,-0,0,-.012,33.052,8.537)"><use xlink:href="#x6C"/></g>

		
	
</svg> during picornavirus replication, we review the evidence and consequence of a host immune response to epitopes in <svg     style="vertical-align:-0.1638pt;width:36.737499px;" id="M4" height="16.9625" version="1.1" viewBox="0 0 36.737499 16.9625" width="36.737499"  xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg">
	
		
			<g transform="matrix(.017,-0,0,-.017,.062,16.7)"><use xlink:href="#x33"/></g><g transform="matrix(.017,-0,0,-.017,8.222,16.7)"><use xlink:href="#x44"/></g>

			<g transform="matrix(.012,-0,0,-.012,20.712,8.537)"><use xlink:href="#x70"/></g><g transform="matrix(.012,-0,0,-.012,27.055,8.537)"><use xlink:href="#x6F"/></g><g transform="matrix(.012,-0,0,-.012,33.052,8.537)"><use xlink:href="#x6C"/></g>

		
	
</svg> after picornavirus infection, highlight data showing the antiviral effects of transgenic <svg     style="vertical-align:-0.1638pt;width:36.737499px;" id="M5" height="16.9625" version="1.1" viewBox="0 0 36.737499 16.9625" width="36.737499"  xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg">
	
		
			<g transform="matrix(.017,-0,0,-.017,.062,16.7)"><use xlink:href="#x33"/></g><g transform="matrix(.017,-0,0,-.017,8.222,16.7)"><use xlink:href="#x44"/></g>

			<g transform="matrix(.012,-0,0,-.012,20.712,8.537)"><use xlink:href="#x70"/></g><g transform="matrix(.012,-0,0,-.012,27.055,8.537)"><use xlink:href="#x6F"/></g><g transform="matrix(.012,-0,0,-.012,33.052,8.537)"><use xlink:href="#x6C"/></g>

		
	
</svg> from Theiler's murine encephalomyelitis virus (TMEV), and discuss potential mechanisms by which <svg     style="vertical-align:-0.1638pt;width:36.737499px;" id="M6" height="16.9625" version="1.1" viewBox="0 0 36.737499 16.9625" width="36.737499"  xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg">
	
		
			<g transform="matrix(.017,-0,0,-.017,.062,16.7)"><use xlink:href="#x33"/></g><g transform="matrix(.017,-0,0,-.017,8.222,16.7)"><use xlink:href="#x44"/></g>

			<g transform="matrix(.012,-0,0,-.012,20.712,8.537)"><use xlink:href="#x70"/></g><g transform="matrix(.012,-0,0,-.012,27.055,8.537)"><use xlink:href="#x6F"/></g><g transform="matrix(.012,-0,0,-.012,33.052,8.537)"><use xlink:href="#x6C"/></g>

		
	
</svg> is causing this antiviral effect in mice.

Jason Kerkvliet

Ramakrishna Edukulla

Moses Rodriguez

Novel Roles of the Picornaviral 3D Polymerase in Viral Pathogenesis

About this journal

<p><em>Advances in Virology</em> publishes articles in all aspect of viruses and viral diseases. Topics covered include viral structure, function, and genetics, as well as virus-host interactions, viral disease outbreaks, and antiviral therapeutics.</p>


Journal profile

Meet the editorial board

<p><em>Advances in Virology</em> maintains an Editorial Board of practicing researchers from around the world, to ensure manuscripts are handled by editors who are experts in the field of study.</p>


Editor spotlight

Submit to Special Issue

We currently have a number of Special Issues open for submission. Special Issues highlight emerging areas of research within a field, or provide a venue for a deeper investigation into an existing research area.

Special Issues

Author guidelines

Editorial board

Databases and indexing

Advances in Virology - Table of contents 2010

title

Advances in Virology publishes articles in all aspect of viruses and viral diseases. Topics covered include viral structure, function, and genetics, as well as virus-host interactions, viral disease outbreaks, and antiviral therapeutics.

Advances in Virology