Codex Mendoza, MS. Arch. Selden. A. 1: Report on repairs of 1985–6, watermarks, collation

This report is not intended as a full physical description of Codex Mendoza. Its purpose is rather to bring together various observations which emerged before, during and after the repairs of 1985–6, about the physical nature of the entire manuscript volume, MS. Arch. Selden. A. 1, in particular about its paper and collation-structure, and to record the minor structural changes made then

Dihydropteroate synthase gene mutations in Pneumocystis and sulfa resistance

Pneumocystis pneumonia (PCP) remains a major cause of illness and death in HIV-infected persons. Sulfa drugs, trimethoprim-sulfamethoxazole (TMP-SMX) and dapsone are mainstays of PCP treatment and prophylaxis. While prophylaxis has reduced the incidence of PCP, its use has raised concerns about development of resistant organisms. The inability to culture human Pneumocystis, Pneumocystis jirovecii, in a standardized culture system prevents routine susceptibility testing and detection of drug resistance. In other microorganisms, sulfa drug resistance has resulted from specific point mutations in the dihydropteroate synthase (DHPS) gene. Similar mutations have been observed in P. jirovecii. Studies have consistently demonstrated a significant association between the use of sulfa drugs for PCP prophylaxis and DHPS gene mutations. Whether these mutations confer resistance to TMP-SMX or dapsone plus trimethoprim for PCP treatment remains unclear. We review studies of DHPS mutations in P. jirovecii and summarize the evidence for resistance to sulfamethoxazole and dapsone

The First In Situ Encounter of Gigantura chuni (Giganturidae: Giganturoidei: Aulopiformes: Cyclosquamata: Teleostei), with a Preliminary Investigation of Pair-Bonding

The Gulf of Mexico Scientific and Environmental ROV Partnership using Existing iNdustrial Technology (Gulf SERPENT) Project utilizes industrial work-class ROVs based at oceanic oil and gas facilities for scientific research and exploration. During Gulf SERPENT operations, an ROV documented the first in situ observations of Gigantura chuni at a depth of approximately 900 m in the northern Gulf of Mexico. The fish were identified to genus by the length of the caudal fin ventral lobe relative to standard length, reflectance from crystalline guanine, and relative mouth size to the head length. The width-length ratios suggest G. chuni as the species (approximately 1:5 for adult G. chuni vs. 1:10 for adult G. indica). The videos provided the second known in situ observation of giganturids and the first of G. chuni. The first video clearly shows two individuals in close proximity, with both oriented vertically in the water column; a second video clip shows a single individual at a slightly shallower depth, and also oriented vertically in the water column. An odds ratio comparison for collections of G. chuni and G. indica from the DEEPEND program to fitted theoretical distributions was used to preliminarily analyze the probability of encountering various numbers of individuals in a single-sample effort. Groups of two individuals, and in particular even number groupings, were encountered during the DEEPEND program sampling more often than would be expected based on theoretical distributions for both G. chuni and G. indica suggesting pair-bonding may be a likely reproductive strategy complementing synchronous hermaphroditism in giganturids

Vaccinia virus immune evasion: mechanisms, virulence and immunogenicity

Virus infection of mammalian cells is sensed by pattern recognition receptors and leads to an innate immune response that restricts virus replication and induces adaptive immunity. In response, viruses have evolved many countermeasures that enable them to replicate and be transmitted to new hosts, despite the host innate immune response. Poxviruses, such as vaccinia virus (VACV), have large DNA genomes and encode many proteins that are dedicated to host immune evasion. Some of these proteins are secreted from the infected cell, where they bind and neutralize complement factors, interferons, cytokines and chemokines. Other VACV proteins function inside cells to inhibit apoptosis or signalling pathways that lead to the production of interferons and pro-inflammatory cytokines and chemokines. In this review, these VACV immunomodulatory proteins are described and the potential to create more immunogenic VACV strains by manipulation of the gene encoding these proteins is discussed

The Genetics of Life and Death: Virus-Host Interactions Underpinning Resistance to African Swine Fever, a Viral Hemorrhagic Disease

Pathogen transmission from wildlife hosts to genetically distinct species is a major driver of disease emergence. African swine fever virus (ASFV) persists in sub-Saharan Africa through a sylvatic cycle between warthogs and soft ticks that infest their burrows. The virus does not cause disease in these animals, however transmission of the virus to domestic pigs or wild boar causes a hemorrhagic fever that is invariably fatal. ASFV transmits readily between domestic pigs and causes economic hardship in areas where it is endemic. The virus is also a significant transboundary pathogen that has become established in Eastern Europe, and has recently appeared in China increasing the risk of an introduction of the disease to other pig producing centers. Although a DNA genome mitigates against rapid adaptation of the virus to new hosts, extended epidemics of African swine fever (ASF) can lead to the emergence of viruses with reduced virulence. Attenuation in the field leads to large deletions of genetic material encoding genes involved in modulating host immune responses. Therefore resistance to disease and tolerance of ASFV replication can be dependent on both virus and host factors. Here we describe the different virus-host interfaces and discuss progress toward understanding the genetic determinants of disease outcome after infection with ASFV

Bat and pig IFN-induced transmembrane protein 3 restrict cell entry by influenza virus and lyssaviruses

IFN-induced transmembrane protein 3 (IFITM3) is a restriction factor that blocks cytosolic entry of numerous viruses that utilize acidic endosomal entry pathways. In humans and mice, IFITM3 limits influenza-induced morbidity and mortality. Although many IFITM3-sensitive viruses are zoonotic, whether IFITMs function as antiviral restriction factors in mammalian species other than humans and mice is unknown. Here, IFITM3 orthologues in the microbat (Myotis myotis) and pig (Sus scrofa domesticus) were identified using rapid amplification of cDNA ends. Amino acid residues known to be important for IFITM3 function were conserved in the pig and microbat orthologues. Ectopically expressed pig and microbat IFITM3 co-localized with transferrin (early endosomes) and CD63 (late endosomes/multivesicular bodies). Pig and microbat IFITM3 restricted cell entry mediated by multiple influenza haemagglutinin subtypes and lyssavirus glycoproteins. Expression of pig or microbat IFITM3 in A549 cells reduced influenza virus yields and nucleoprotein expression. Conversely, small interfering RNA knockdown of IFITM3 in pig NPTr cells and primary microbat cells enhanced virus replication, demonstrating that these genes are functional in their species of origin at endogenous levels. In summary, we showed that IFITMs function as potent broad-spectrum antiviral effectors in two mammals – pigs and bats – identified as major reservoirs for emerging viruses