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PubMed2005

Optimal duration of PET studies with 18F-fluoroethyl-diprenorphine.

UNLABELLED: The tracer 6-O-(2-(18)F-fluoroethyl)-6-O-desmethyldiprenorphine (18F-FDPN) provides enhanced flexibility to PET studies of the opioidergic system because the label has a longer half-life than the label of 11C-diprenorphine. Here we evaluated the ideal length of PET studies with 18F-FDPN. METHODS: 18F-FDPN binding kinetics were quantified with protocols of different lengths by use of a 1-tissue or a 2-tissue compartment model for different volumes of interest. Furthermore, the effects of scanning duration were assessed by parametric analyses. RESULTS: A 90-min protocol resulted in less than 10% bias in distribution volume (DV) relative to the full-length protocol. Correlation analyses of the DV estimates for the full-length protocol and the shortened protocols showed good replication of DV estimates for regions with both low and high levels of binding at schedules of up to 90 min. CONCLUSION: Data sampling in dynamic 18F-FDPN PET acquisitions should not be shorter than 90 min to maintain reliable estimates of DV.

Adult↗
PubMed2002

Intestinal stem cells protect their genome by selective segregation of template DNA strands.

The stem cells in the crypts of the small intestinal mucosa divide about a thousand times during the lifespan of a laboratory mouse, and yet they show little evidence of any decline in proliferative potential and rarely develop carcinogenic mutations, suggesting that their genome is extremely well protected. Protection against DNA-replication-induced errors can be achieved by the selective sorting of old (template) and new DNA strands with all template strands retained in the stem cell line. The template strands in the stem cells can be labelled during development or during tissue regeneration using tritiated thymidine ((3)HTdR). Labelling newly synthesised strands with a different marker (bromodeoxyuridine, BrdUrd) allows segregation of the two markers to be studied. Template strand label is retained ((3)HTdR), whereas label in the newly synthesised strands (BrdUrd) is lost following the second division of the stem cell. Random errors may occur in the template strands owing to environmental elements. These are protected against by the altruistic cell suicide (apoptosis) of the cells incurring such errors. A final level of protection for the tissue compensates for excessive deletion of stem cells via the apoptosis pathway. This is achieved by a hierarchical age structure in the stem cell compartment, with some cells being able to efficiently repair DNA damage and hence being more radioresistant. The presence of these protective mechanisms ensures that the small intestine rarely develops cancer and that stem cells can sustain the extensive cell proliferation needed during life.

Animals↗
PubMed2000

Partitioning of the linear chromosome during sporulation of Streptomyces coelicolor A3(2) involves an oriC-linked parAB locus.

Candidate partitioning genes (parA and parB) for the linear chromosome of Streptomyces coelicolor were identified by DNA sequencing in a series of seven genes located between rnpA and trxA near the chromosomal replication origin. The most likely translation start point of parB overlapped the parA stop codon, suggestive of coregulation, and transcription analysis suggested that the two genes formed an operon. Deletion of part of parB had no effect on the growth or appearance of colonies but caused a deficiency in DNA partitioning during the multiple septation events involved in converting aerial hyphae into long chains of spores. At least 13% of spore compartments failed to inherit the normal DNA allocation. The same phenotype was obtained with a deletion removing a segment of DNA from both parA and parB. Reinforcing the idea of a special role for the par locus during sporulation, the stronger of two parAB promoters was greatly upregulated at about the time when sporulation septation was maximal in colonies. Three copies of a 14-bp inverted repeat (GTTTCACGTGAAAC) were found in or near the parAB genes, and at least 12 more identical copies were identified within 100 kb of oriC from the growing genome sequence database. Only one perfect copy of the 14-bp sequence was present in approximately 5 Mb of sequence available from the rest of the genome. The 14-bp sequence was similar to sequences identified as binding sites for Spo0J, a ParB homologue from Bacillus subtilis believed to be important for DNA partitioning (D. C.-H. Lin and A. D. Grossman, Cell 92:675-685, 1998). One of these sites encompassed the transcription start point of the stronger parA promoter.

Amino Acid Sequence↗
PubMed2004

Inseminated female mice (Mus musculus) investigate rather than avoid novel males that disrupt pregnancy, but sires protect pregnancy.

Experiment 1 replicated the Bruce effect, showing pregnancy termination in CF1 strain female mice (Mus musculus) housed underneath novel heterogeneous strain (HS) males. In a 4-arm maze in Experiment 2, inseminated CF1 females approached novel HS males more often than CF1 sires or unfamiliar CF1 males. In Experiment 3, inseminated females showed random nesting sites when housed continuously underneath 4 compartments containing the sire, a novel CF1 male, a novel HS male, and no stimulus. In Experiment 4, when inseminated females were housed with or without the sire below novel HS males, the sire's presence decreased female interaction with novel males and mitigated the Bruce effect. Inseminated females do not reliably avoid males that disturb pregnancy unless the sire is immediately present.

Animals↗
PubMed1996

Cell killing by the novel imidazoacridinone antineoplastic agent, C-1311, is inhibited at high concentrations coincident with dose-differentiated cell cycle perturbation.

We have studied the actions of C-1311, an imidazoacridinone analogue with potent in vivo antitumour activity, against a human tumour line (HeLa S3), in an examination of the events associated with the lethality of this agent. Continuous exposures (24 h) induced complete G2 arrest, although the concentration range of this effect was narrow, with elevation of the drug level inducing additional and increasing impediment to S-phase transit. Acute treatments (3 h) revealed that cells exposed to drug levels, which first induced persistent G2 arrest (0.5 microgram ml-1), subsequently died from this compartment, while doses exceeding these levels (1.0 microgram ml-1), paradoxically, did not cause the same extensive cell death. We explain our findings on the proposition that this particular mode of cell death is dependent upon inappropriate activation of the primed mitotic machinery-specifically the hyperphosphorylated p34cdc2/cyclin B complex-assembled within G2, but that impediment to genomic replication at higher doses inhibits assembly of this complex, and hence prevents cell death. Our results demonstrate that high dose does not necessarily correlate with increased cell death, while at the same time providing further evidence for the importance of events normally associated with the G2/M transition in DNA damage-induced tumour cell death.

Aminoacridines↗
PubMed1997

Telomerase activity concentrates in the mitotically active segments of human hair follicles.

Telomerase is a ribonucleoprotein enzyme capable of adding hexanucleotide repeats onto the ends of linear chromosomal DNA. Whereas normal somatic cells with a limited replicative capacity fail to express telomerase activity, most immortal eukaryotic cells do. Cells of renewal tissues (e.g., skin, intestine, blood) require an extensive proliferative capacity. Some cells in such renewal tissues also express telomerase activity, most likely to prevent rapid erosion of their telomeres during cell proliferation. In this study, we measured the levels of telomerase activity in dissected compartments of the human hair follicle: hair shaft, gland-containing fragment, upper intermediate fragment (where it is thought undifferentiated stem cells reside), lower intermediate fragment, and in the bulb-containing fragment (an area with high mitotic activity containing a more differentiated pool of keratinocytes). In anagen follicles, high levels of telomerase activity were found almost exclusively in the bulb-containing fragment of the follicles, with low levels of telomerase in the bulge area (intermediate fragments) and gland-containing fragment. In comparison, catagen follicles had low levels of telomerase activity in the bulb-containing fragments as well as in other compartments. Such observations indicate that, in anagen hair follicles, the fragments containing cells actively dividing (e.g., transient amplifying cells) express telomerase activity, whereas fragments containing cells with low mitotic activity, for example, quiescent stem cells, express low levels of telomerase activity.

Adult↗
PubMed1980

Perturbation of cell cycle progression in mouse epidermis prior to the regenerative response.

Cell kinetic perturbations that resulted in a wave of increased cell division during the 6--8 hr lag period prior to regenerative DNA replication in mouse epidermis were examined. The epidermis was stimulated to proliferate by adhesive tape stripping, and flow cytometric DNA measurements of isolated epidermal basal cells, counting of mitoses, of Colcemid arrested metaphases and of labeled mitoses among basal cells in histologic sections were made. The results showed that mitotic peaks that occur in the pre-replicative period subsequent to tape stripping can be explained by a delay in cell progression through the S phase, followed by subsequent release and partial synchrony in further cell cycle progression. Early peaks of mitoses in epidermis stimulated to proliferate should therefore not, without further evidence, be assumed to originate from cells triggered into division from a resting G2 compartment. The results also indicate an initial delayed cell progression through the G2 phase, whereas the mitotic duration seemed to be initially reduced, indicating that the DNA synthesis phase and the G2 phase are parts of the epidermal cell cycle that may be most vulnerable to various types of influences.

Animals↗
PubMed2005

Population pharmacokinetics of epinastine, a histamine H1 receptor antagonist, in adults and children.

AIMS: Our objective was to develop a population pharmacokinetic (PPK) model for epinastine, a histamine H(1) receptor antagonist, in adults and children and to obtain pharmacokinetic information to support dosing recommendations in children. METHODS: A total of 1510 plasma samples were collected from 62 healthy adult volunteers and 62 paediatric atopic dermatitis patients. The data were analysed using the NONMEM program according to a two-compartment model with first-order absorption. In addition, the final PPK model was evaluated by means of bootstrapping resampling. RESULTS: The oral clearance (CL/F) was found to be associated with body weight, formulation and food status. The volume of distribution of the central compartment (V(1)/F) was related to body weight and food status. An absorption lag time was apparent in fed subjects. On the other hand, other covariates (formulation on V(1)/F, volume of distribution of the peripheral compartment (V(2)/F), first-order absorption rate constant (Ka) and absorption lag time (ALAG); food status on V(2)/F and Ka; body weight on V(2)/F) were not statistically significant. No effect of age on CL/F, V(1)/F or V(2)/F was found. The mean parameter estimates obtained with an additional 200 bootstrap replicates of data were within 90-117% of those obtained with the original data set. These results suggest that the pharmacokinetics of epinastine are similar in adults and in children, except for the effect of the difference of body weight. The result of the application of the PPK model to the clinical trial in paediatric patients, in which dosage was determined based on the body weight (from 14 kg to less than 24 kg; 10 mg dose, 24 kg or more; 20 mg dose), showed that the C(max) and AUC (25.6 +/- 6.9 ng ml(-1) and 246.8 +/- 68.2 ng h ml(-1)) were almost same levels with those of adults after administration of 20 mg (26.9 +/- 9.1 ng ml(-1) and 281.6 +/- 90.5 ng h ml(-1)). CONCLUSIONS: A PPK model for epinastine was established and further evaluation by bootstrapping indicated that this model is stable. The model shows that, if dosage is adjusted based on the body weight, the epinastine exposure in paediatric patients is similar to that in adults.

Adult↗
PubMed2005

Dual effect of the SR proteins ASF/SF2, SC35 and 9G8 on HIV-1 RNA splicing and virion production.

In HIV-1 infected cells transcription of the integrated provirus generates the single full length 9 kb viral RNA, a major fraction of which is spliced to produce the single-spliced 4 kb RNAs and the multiple-spliced 2 kb RNAs. These spliced RNAs are the messengers for the Env glycoproteins and the viral regulatory factors. The cellular SR and hnRNP proteins were shown in vitro to control alternative splicing by binding cis-regulatory elements on the viral RNA. To better understand in vivo the role of the SR proteins on HIV-1 genomic RNA splicing and virion production, we used a human cell line expressing high levels of complete HIV-1 and either one of the ASF/SF2, SC35, and 9G8 SR proteins. Results show that over-expressing SR proteins caused a large reduction of genomic RNA and that each SR protein modified the viral 9 kb RNA splicing pattern in a specific mode. In fact, ASF/SF2 increased the level of Vpr RNA while SC35 and 9G8 caused a large increase in Tat RNA. As expected, overexpressing SR proteins caused a strong reduction of total Gag made. However, we observed by immuno-confocal microscopy an accumulation of Gag at the plasma membrane and in intracellular compartments while there is a dramatic reduction of Env protein made in most cells. Due to the negative impact of the SR proteins on the levels of genomic RNA and HIV-1 structural proteins much less virions were produced which retained part of their infectivity. In conclusion, SR proteins can down-regulate the late steps of HIV-1 replication.

Cell Line↗
PubMed1997

Immunity to PRRSV: double-edged sword.

The immune system is a double-edged sword for porcine reproductive and respiratory syndrome virus (PRRSV) infection. On one edge PRRSV has a predilection for immune cells and the disease manifestations can be linked directly to changes in the immune system. PRRSV appears to replicate extensively, if not exclusively, in cells of the immune lineage, notably macrophages; the direct replication of which may lead to immunosuppression, precipitate secondary infection and/or mediate disease. On the other edge, the virus stimulates immunity post-infection that protects an animal from re-infection. A vast array of structural and functionally distinct antibody specific to PRRSV are generated following infection or vaccination. Discrete populations of functional antibodies appear at different times and possibly reflect reactivity to different PRRSV polypeptides. Cell-mediated immune responses specific to PRRSV can be detected in various exposed pigs as well. Thus, the immune system appears to be intimately involved in both the disease process and protection from disease. It is unclear at this state of understanding what immune compartment provides protective immunity. It is humoral (i.e. antibodies), selective functionally distinct populations of antibodies specific for selected PRRSV polypeptides or is cellular immunity essential for protection, or both. This review will attempt to summarize the current state of knowledge of the complex interaction of the immune system and PRRSV.

Animals↗
PubMed2003

Cell cycle events during the development of the silk glands in the mulberry silkworm Bombyx mori.

Silk glands of the mulberry silkworm Bombyx mori are long and paired structures originating from the labial region and are anatomically and physiologically divided into three major compartments, the anterior, middle and posterior silk glands. The silk gland morphogenesis is complete by 8 days post egg laying. Extensive growth of silk glands during the larval stages is due to increase in tissue mass and not cell number. The cells in a completely formed silk gland pursue an endoreplicative cell cycle, and the genome undergoes multiple rounds of replication without mitosis or nuclear division. The expression patterns of cyclin B (mitotic cyclin) and cyclin E (G1 cyclin, essential for G1/S transition in both mitotic and endoreplicative cell cycles) in the course of silk gland development revealed that mitotic cell divisions take place only in the apex of the growing silk gland. However, the persistence of another mitotic focus in the middle silk gland even when the growing apex has moved well past this zone suggested the continued operation of mitosis for a while in this restricted region. The lack of cyclin B expression and abundance of cyclin E in the rest of the areas confirmed an alternation of the G1 and S phases of the cell cycle without an intervening mitotic phase. No expression of cyclin B was noticed anywhere in the silk glands after stage 25 of embryogenesis, indicating a complete switch over to the endomitotic mode of the cell cycle. The onset of expression of various genes encoding different silk proteins correlated with the onset of endomitotic events.

Animals↗
PubMed2000

Incorporation of nucleoside analogs into nuclear or mitochondrial DNA is determined by the intracellular phosphorylation site.

Nucleoside analogs used in cancer chemotherapy and in treatment of virus infections are phosphorylated in cells by nucleoside and nucleotide kinases to their pharmacologically active form. The phosphorylated nucleoside analogs are incorporated into DNA and cause cell death or inhibit viral replication. Cellular DNA is replicated both in the nucleus and in the mitochondria, and nucleoside analogs may interfere with DNA replication in both these subcellular locations. In the present study we created a cell model system where nucleoside analogs were phosphorylated, and thereby pharmacologically activated, in either the nucleus, cytosol, or mitochondria of cancer cells. The system was based on the reconstitution of deoxycytidine kinase (dCK)-deficient Chinese hamster ovary cells with genetically engineered dCK targeted to the different subcellular compartments. The nucleoside analogs phosphorylated by dCK in the mitochondria were predominantly incorporated into mitochondrial DNA, whereas the nucleoside analogs phosphorylated in the nucleus or cytosol were incorporated into nuclear DNA. We further show that the nucleoside analogs phosphorylated in the mitochondria induced cell death by an apoptotic program. These data showed that the subcellular site of nucleoside analog phosphorylation is an important determinant for incorporation of nucleoside analogs into nuclear or mitochondrial DNA.

Amino Acid Sequence↗
PubMed2006

Three-dimensional reconstruction of the membrane skeleton at the plasma membrane interface by electron tomography.

Three-dimensional images of the undercoat structure on the cytoplasmic surface of the upper cell membrane of normal rat kidney fibroblast (NRK) cells and fetal rat skin keratinocytes were reconstructed by electron tomography, with 0.85-nm-thick consecutive sections made approximately 100 nm from the cytoplasmic surface using rapidly frozen, deeply etched, platinum-replicated plasma membranes. The membrane skeleton (MSK) primarily consists of actin filaments and associated proteins. The MSK covers the entire cytoplasmic surface and is closely linked to clathrin-coated pits and caveolae. The actin filaments that are closely apposed to the cytoplasmic surface of the plasma membrane (within 10.2 nm) are likely to form the boundaries of the membrane compartments responsible for the temporary confinement of membrane molecules, thus partitioning the plasma membrane with regard to their lateral diffusion. The distribution of the MSK mesh size as determined by electron tomography and that of the compartment size as determined from high speed single-particle tracking of phospholipid diffusion agree well in both cell types, supporting the MSK fence and MSK-anchored protein picket models.

Actin Cytoskeleton↗
PubMed2003

Simian immunodeficiency virus Nef gene regulates the production of 2-LTR circles in vivo.

The replication dynamics of simian immunodeficiency virus (SIVmac32H-C8), attenuated through discrete genetic disruption of the nef gene, were compared with the wild-type parental clone (SIVmac32H-J5) using quantitative molecular methods. The primary viraemia of both infections were similar during the first week, but peaked on Day 10 at higher levels for wild-type virus. Viral RNA levels differed most markedly at Day 14. The frequency and levels of viral DNA species, detectable as gag provirus or circular 2-LTR episomes, differed depending on the virus and the lymphoid compartment sampled. 2-LTR circles persisted for prolonged periods in the peripheral blood but were never detected in any SIVmac32H C8-infected tissue, even if positive by gag PCR. Paradoxically, the converse was observed following wild-type infection. 2-LTR circles disappeared from the peripheral blood by Day 42 postinfection but persisted in lymphoid tissues. These findings are discussed in terms of nef and the role and stability of 2-LTR circle forms in vivo.

Animals↗
PubMed1998

Exclusive and persistent use of the entry coreceptor CXCR4 by human immunodeficiency virus type 1 from a subject homozygous for CCR5 delta32.

Individuals who are homozygous for the 32-bp deletion in the gene coding for the chemokine receptor and major human immunodeficiency virus type 1 (HIV-1) coreceptor CCR5 (CCR5 -/-) lack functional cell surface CCR5 molecules and are relatively resistant to HIV-1 infection. HIV-1 infection in CCR5 -/- individuals, although rare, has been increasingly documented. We now report that the viral quasispecies from one such individual throughout disease is homogenous, T cell line tropic, and phenotypically syncytium inducing (SI); exclusively uses CXCR4; and replicates well in CCR5 -/- primary T cells. The recently discovered coreceptors BOB and Bonzo are not used. Although early and persistent SI variants have been described in longitudinal studies, this is the first demonstration of exclusive and persistent CXCR4 usage. With the caveat that the earliest viruses available from this subject were from approximately 4 years following primary infection, these data suggest that HIV-1 infection can be mediated and persistently maintained by viruses which exclusively utilize CXCR4. The lack of evolution toward the available minor coreceptors in this subject underscores the dominant biological roles of the major coreceptors CCR5 and CXCR4. This and two similar subjects (R. Biti, R. Ffrench, J. Young, B. Bennetts, G. Stewart, and T. Liang, Nat. Med. 3:252-253, 1997; I. Theodoreu, L. Meyer, M. Magierowska, C. Katlama, and C. Rouzioux, Lancet 349:1219-1220, 1997) showed relatively rapid CD4+ T-cell declines despite average or low initial viral RNA load. Since viruses which use CXCR4 exclusively cannot infect macrophages, these data have implications for the relative infection of the T-cell compartment versus the macrophage compartment in vivo and for the development of CCR5-based therapeutics.

Acquired Immunodeficiency Syndrome↗
PubMed2006

HIV-1 infection downregulates nuclear telomerase activity on lymphoblastoic cells without affecting the enzymatic components at the transcriptional level.

Both increased lymphocyte renewal with subsequent exhaustion of the immune system and impaired T cell renewal have been put into view to account for CD4+ T cell depletion and development of AIDS in HIV-1- infected humans. Telomerase is an enzyme that is involved in mechanisms that control cell life span and replicative potential. The effect of HIV-1 on telomerase activity, certain regulators, and telomeric terminal restriction fragment length on lymphoid Jurkat cells was used in measuring the proliferative activity of T lymphoid cells before and after being infected. At the cellular level, the enzymatic activity remains almost stable but further analyses of fractionated cells revealed that telomerase activity in the nuclear compartment was diminished whereas in the cytoplasmic compartment it was relatively increased on HIV-1 infection. Two key components of telomerase regulation were further considered at the transcriptional level, that is, the mRNA levels of both human telomerase reverse transcriptase (hTERT)--including the relative amount of its alternative splicing variants--and hTR. They were unaffected on HIV-1 infection. Telomeric length was also conserved in infected cells. Overall, these findings demonstrate that HIV-1 infection of Jurkat cells down modulate telomerase activity in the nuclear compartment by affecting its cellular localization.

Cell Nucleus↗
PubMed2002

A modelling study of locomotion-induced hyperpolarization of voltage threshold in cat lumbar motoneurones.

During fictive locomotion the excitability of adult cat lumbar motoneurones is increased by a reduction (a mean hyperpolarization of approximately 6.0 mV) of voltage threshold (Vth) for action potential (AP) initiation that is accompanied by only small changes in AP height and width. Further examination of the experimental data in the present study confirms that Vth lowering is present to a similar degree in both the hyperpolarized and depolarized portions of the locomotor step cycle. This indicates that Vth reduction is a modulation of motoneurone membrane currents throughout the locomotor state rather than being related to the phasic synaptic input within the locomotor cycle. Potential ionic mechanisms of this locomotor-state-dependent increase in excitability were examined using three five-compartment models of the motoneurone innervating slow, fast fatigue resistant and fast fatigable muscle fibres. Passive and active membrane conductances were set to produce input resistance, rheobase, afterhyperpolarization (AHP) and membrane time constant values similar to those measured in adult cat motoneurones in non-locomoting conditions. The parameters of 10 membrane conductances were then individually altered in an attempt to replicate the hyperpolarization of Vth that occurs in decerebrate cats during fictive locomotion. The goal was to find conductance changes that could produce a greater than 3 mV hyperpolarization of Vth with only small changes in AP height (< 3 mV) and width (< 1.2 ms). Vth reduction without large changes in AP shape could be produced either by increasing fast sodium current or by reducing delayed rectifier potassium current. The most effective Vth reductions were achieved by either increasing the conductance of fast sodium channels or by hyperpolarizing the voltage dependency of their activation. These changes were particularly effective when localized to the initial segment. Reducing the conductance of delayed rectifier channels or depolarizing their activation produced similar but smaller changes in Vth. Changes in current underlying the AHP, the persistent Na(+) current, three Ca(2+) currents, the "h" mixed cation current, the "A" potassium current and the leak current were either ineffective in reducing Vth or also produced gross changes in the AP. It is suggested that the increased excitability of motoneurones during locomotion could be readily accomplished by hyperpolarizing the voltage dependency of fast sodium channels in the axon hillock by a hitherto unknown neuromodulatory action.

Animals↗
PubMed2006

Sequence requirements for localization of human cytomegalovirus tegument protein pp28 to the virus assembly compartment and for assembly of infectious virus.

The human cytomegalovirus UL99 open reading frame encodes a 190-amino-acid (aa) tegument protein, pp28, that is myristoylated and phosphorylated. pp28 is essential for assembly of infectious virus, and nonenveloped virions accumulate in the cytoplasm of cells infected with recombinant viruses with a UL99 deletion. pp28 is localized to the endoplasmic reticulum-Golgi intermediate compartment (ERGIC) in transfected cells, while in infected cells, it is localized together with other virion proteins in a juxtanuclear compartment termed the assembly compartment (AC). We investigated the sequence requirements for pp28 trafficking to the AC and assembly of infectious virus. Our studies indicated that the first 30 to 35 aa were required for localization of pp28 to the ERGIC in transfected cells. Mutant forms of pp28 containing only the first 35 aa localized with other virion structural proteins to cytoplasmic compartments early in infection, but localization to the AC at late times required a minimum of 50 aa. In agreement with previous reports, we demonstrated that the deletion of a cluster of acidic amino acids (aa 44 to 59) prevented wild-type trafficking of pp28 and recovery of infectious virus. A recombinant virus expressing only the first 50 aa was replication competent, and this mutant, pp28, localized to the AC in cells infected with this virus. These findings argued that localization of pp28 to the AC was essential for assembly of infectious virus and raised the possibility that amino acids in the amino terminus of pp28 have additional roles in the envelopment and assembly of the virion other than simply localizing pp28 to the AC.

Animals↗