What is the life cycle of a wart?

There doesn't seem to be a lot of information available on research done on warts. What is the life cycle of a wart? How does it spread? -- specifically how does it recruit cells to spread it? What is the life cycle of a PV-infected dermal cell?

This article has some good information. It's certainly more than I want to know about warts.

Isolated warts may remain unaltered for months or years, or a large number of new lesions may develop rapidly in a short period of time. The development of warts is not predictable. Approximately 65% of warts disappear spontaneously within two years. The patient's age and number of lesions do not seem to affect the prognosis.

There are many different types of warts and of HPV. Since warts cause a type of dysplasia their life cycle can be very variable and unpredictable.

Conner's response contained just the type of source material I was looking for. Thanks Conner -- let us all +1 him. Allow me to summarize the specifics of the article in relation to my question:


PVs are transmitted through direct or indirect contact with an individual who has the lesion. Dysfunctions in the epithelial barrier by trauma, minor injuries or maceration cause loss of solution of continuity in the skin, thus allowing viral infection. After inoculation, the incubation period varies from 3 weeks to 8 months. Spontaneous regression is observed in most cases.


Infection begins when the PV reaches the cells of the basal layer; there is no viral replication at this location and the virus just keeps its genome by amplification of a low number of copies.


The replicative phase and protein synthesis occur in the suprabasal differentiated keratinocytes. Progression time and type of lesion correlates with the quantity of viral particles detected. Younger warts present a higher viral amount when compared to old warts. Plantar warts have a higher viral load than common warts. The center of the lesion appears to be the main site of viral concentration.


PVs appear to remain in their host for long periods of life. A variety of different types of PVs can be detected in random sites of normal skin in humans and animals. This reinforces that a latent life cycle is often a characteristic of these viruses.

Interesting Notes

  • There are no known PVs that infect more than one species.
  • To date, about 100 different types of HPVs have been fully characterized.
  • Human PVs does not grow on conventional culture media. The diagnosis of HPV infection is made by histopathology of lesions

Slug Portal

Deroceras reticulatum Müller, the gray field slug (or sometimes called gray garden slug), has many different adult color morphs and damages multiple crops in the Pacific Northwest (PNW) and worldwide. In the Willamette Valley, D. reticulatum comprises more than 90% of the slugs found in grasses grown for seed. All but one of the slug species (Prophysaon andersoni) found in grasses grown for seed are invasive or exotic. This species is an important agricultural pest in the family Agriolimacidae. Note the position of the pneumostome, the short keel at the back of the body, the mucous which is typically colorless but turns white when the slug is disturbed. Deroceras reticulatum is the only Deroceras species in the US that can change its mucous from colorless to milkey. As far as habitat choice, the gray field slug chooses cultivated areas such as agricultural field crops, backyard gardens, roadside, parks, and meadows. This slug is much less common in natural habitats like forests. It is native to Europe, North Africa and the Atlantic Islands.

ADULTS: Slugs are hermaphrodites—every slug is born with both male and female reproductive parts and any slug is capable of laying eggs, though self-fertilization can occur. In the temperate climate of the PNW, mating typically is observed in the fall (Oct-Nov) and continues in the spring (Mar-Jun). When a slug matures, which can take approximately 5-6 months over the winter, it weighs more than 200 mg (up to 500mg) and now has the capacity to produce eggs. When in motion, it is about 35 to 50 mm (> 1.5 inches long). Adult slugs overwinter and can lay clutches of eggs when environmental conditions are right. A slug’s life expectancy is from 6 to 12 months, and some up to 18 months. Two generations of the gray field slug are possible in PNW, although information on biology is limited.

EGGS: Small, round, pearl-like, translucent (younger) eggs are laid in clusters of a dozen or more (over 500 eggs in a lifetime average 40 eggs/cluster) in sheltered cavities near the soil surface or under residue on the soil surface, if the soil is moist. As eggs mature they turn white and can take from 2 weeks to a month to hatch, depending on the environmental conditions. It can take 5 months to hatch if eggs are laid late winter. Mature adults deposit eggs late in the season, often after mid-October. If that is the case, the eggs will overwinter, and may not hatch until the following spring. The greatest egg- laying activity in non-irrigated environments usually occurs soon after the first fall rains before temperature declines.

NEONATES: A newly-hatched slug is called a neonate, and their typical food of choice is algae and fungus. However, they can feed on vegetative parts of plants. Young neonates weigh between 1-10 mg. They don’t travel far from home.

JUVENILES: Juvenile slugs will begin feeding throughout the spring and sometimes in the summer, if moisture is present and it is not too hot. If conditions are unsuitable, juveniles and adults will rest (aestivate) under clods and debris, in burrows and soil cracks. Aestivation is a physiological response of slugs under challenging times of environmental adversity, like dryness, summer heat, scarcity of food. They are known to survive without food for several months. Juveniles weigh between 11-100 mg.


  • Subfamily Alphaherpesvirinae
    • Iltovirus
    • Mardivirus
    • Scutavirus
    • Simplexvirus
    • Varicellovirus
    • Cytomegalovirus
    • Muromegalovirus
    • Proboscivirus
    • Quwivirus
    • Roseolovirus
    • Bossavirus
    • Lymphocryptovirus
    • Macavirus
    • Manticavirus
    • Patagivirus
    • Percavirus
    • Rhadinovirus

    Additionally, the species Iguanid herpesvirus 2 is currently unassigned to a genus and subfamily. [6]

    See Herpesvirales#Taxonomy for information on taxonomic history, phylogenetic research, and the nomenclatural system.

    All members of the Herpesviridae share a common structure a relatively large, monopartite, double-stranded, linear DNA genome encoding 100-200 genes encased within an icosahedral protein cage (with T=16 symmetry) called the capsid, which is itself wrapped in a protein layer called the tegument containing both viral proteins and viral mRNAs and a lipid bilayer membrane called the envelope. This whole particle is known as a virion. The structural components of a typical HSV virion are the Lipid bilayer envelope, Tegument, DNA, Glycoprotein spikes and Nucleocapsid. The four-component Herpes simplex virion encompasses the double-stranded DNA genome into an icosahedral nucleocapsid. There is tegument around. Tegument contains filaments, each 7 nm wide. It is an amorphous layer with some structured regions. Finally, it is covered with a lipoprotein envelope. There are spikes made of glycoprotein protruding from each virion. These can expand the diameter of the virus to 225 nm. The diameters of virions without spikes are around 186 nm. There are at least two unglycosylated membrane proteins in the outer envelope of the virion. There are also 11 glycoproteins. These are gB, gC, gD, gE, gG, gH, gI, gJ, gK, gL and gM. Tegument contains 26 proteins. They have duties such as capsid transport to the nucleus and other organelles, activation of early gene transcription, and mRNA degradation. The icosahedral nucleocapsid is similar to that of tailed bacteriophage in the order Caudovirales. This capsid has 161 capsomers consisting of 150 hexons and 11 pentons, as well as a portal complex that allows entry and exit of DNA into the capsid. [12] [13]

    All herpesviruses are nuclear-replicating—the viral DNA is transcribed to mRNA within the infected cell's nucleus.

    Infection is initiated when a viral particle contacts a cell with specific types of receptor molecules on the cell surface. Following binding of viral envelope glycoproteins to cell membrane receptors, the virion is internalized and dismantled, allowing viral DNA to migrate to the cell nucleus. Within the nucleus, replication of viral DNA and transcription of viral genes occurs.

    During symptomatic infection, infected cells transcribe lytic viral genes. In some host cells, a small number of viral genes termed latency-associated transcript (LAT) accumulate, instead. In this fashion, the virus can persist in the cell (and thus the host) indefinitely. While primary infection is often accompanied by a self-limited period of clinical illness, long-term latency is symptom-free.

    Chromatin dynamics regulate the transcription competency of entire herpes virus genomes. When the virus enters a cell, the cellular immune response is to protect the cell. The cell does so by wrapping the viral DNA around histones and condensing it into chromatin, causing the virus to become dormant, or latent. If cells are unsuccessful and the chromatin is loosely bundled, the viral DNA is still accessible. The viral particles can turn on their genes and replicate using cellular machinery to reactivate, starting a lytic infection. [14]

    Reactivation of latent viruses has been implicated in a number of diseases (e.g. shingles, pityriasis rosea). Following activation, transcription of viral genes transitions from LAT to multiple lytic genes these lead to enhanced replication and virus production. Often, lytic activation leads to cell death. Clinically, lytic activation is often accompanied by emergence of nonspecific symptoms, such as low-grade fever, headache, sore throat, malaise, and rash, as well as clinical signs such as swollen or tender lymph nodes and immunological findings such as reduced levels of natural killer cells.

    In animal models, local trauma and system stress have been found to induce reactivation of latent herpesvirus infection. Cellular stressors like transient interruption of protein synthesis and hypoxia are also sufficient to induce viral reactivation. [15]

    Genus Subfamily Host details Tissue tropism Entry details Release details Replication site Assembly site Transmission
    Iltovirus α Birds: galliform: psittacine None Cell receptor endocytosis Budding Nucleus Nucleus Oral-fecal, aerosol
    Proboscivirus β Elephants None Glycoproteins Budding Nucleus Nucleus Contact
    Cytomegalovirus β Humans monkeys Epithelial mucosa Glycoproteins Budding Nucleus Nucleus Urine, saliva
    Mardivirus α Chickens turkeys quail None Cell receptor endocytosis Budding Nucleus Nucleus Aerosol
    Rhadinovirus γ Humans mammals B-lymphocytes Glycoproteins Budding Nucleus Nucleus Sex, saliva
    Macavirus γ Mammals B-lymphocytes Glycoproteins Budding Nucleus Nucleus Sex, saliva
    Roseolovirus β Humans T-cells B-cells NK-cell monocytes macrophages epithelial Glycoproteins Budding Nucleus Nucleus Respiratory contact
    Simplexvirus α Humans mammals Epithelial mucosa Cell receptor endocytosis Budding Nucleus Nucleus Sex, saliva
    Scutavirus α Sea turtles None Cell receptor endocytosis Budding Nucleus Nucleus Aerosol
    Varicellovirus α Mammals Epithelial mucosa Glycoproteins Budding Nucleus Nucleus Aerosol
    Percavirus γ Mammals B-lymphocytes Glycoproteins Budding Nucleus Nucleus Sex, saliva
    Lymphocryptovirus γ Humans mammals B-lymphocytes Glycoproteins Budding Nucleus Nucleus Saliva
    Muromegalovirus β Rodents Salivary glands Glycoproteins Budding Nucleus Nucleus Contact

    The three mammalian subfamilies – Alpha-, Beta- and Gamma-herpesviridae – arose approximately 180 to 220 mya. [16] The major sublineages within these subfamilies were probably generated before the mammalian radiation of 80 to 60 mya. Speciations within sublineages took place in the last 80 million years probably with a major component of cospeciation with host lineages.

    All the currently known bird and reptile species are alphaherpesviruses. Although the branching order of the herpes viruses has not yet been resolved, because herpes viruses and their hosts tend to coevolve this is suggestive that the alphaherpesviruses may have been the earliest branch.

    The time of origin of the genus Iltovirus has been estimated to be 200 mya while those of the mardivirus and simplex genera have been estimated to be between 150 and 100 mya. [17]

    Herpesviruses are known for their ability to establish lifelong infections. One way this is possible is through immune evasion. Herpesviruses have many different ways of evading the immune system. One such way is by encoding a protein mimicking human interleukin 10 (hIL-10) and another is by downregulation of the major histocompatibility complex II (MHC II) in infected cells.

    CmvIL-10 Edit

    Research conducted on cytomegalovirus (CMV) indicates that the viral human IL-10 homolog, cmvIL-10, is important in inhibiting pro-inflammatory cytokine synthesis. The cmvIL-10 protein has 27% identity with hIL-10 and only one conserved residue out of the nine amino acids that make up the functional site for cytokine synthesis inhibition on hIL-10. There is, however, much similarity in the functions of hIL-10 and cmvIL-10. Both have been shown to down regulate IFN-γ, IL-1α, GM-CSF, IL-6 and TNF-α, which are all pro-inflammatory cytokines. They have also been shown to play a role in downregulating MHC I and MHC II and up regulating HLA-G (non-classical MHC I). These two events allow for immune evasion by suppressing the cell-mediated immune response and natural killer cell response, respectively. The similarities between hIL-10 and cmvIL-10 may be explained by the fact that hIL-10 and cmvIL-10 both use the same cell surface receptor, the hIL-10 receptor. One difference in the function of hIL-10 and cmvIL-10 is that hIL-10 causes human peripheral blood mononuclear cells (PBMC) to both increase and decrease in proliferation whereas cmvIL-10 only causes a decrease in proliferation of PBMCs. This indicates that cmvIL-10 may lack the stimulatory effects that hIL-10 has on these cells. [18]

    It was found that cmvIL-10 functions through phosphorylation of the Stat3 protein. It was originally thought that this phosphorylation was a result of the JAK-STAT pathway. However, despite evidence that JAK does indeed phosphorylate Stat3, its inhibition has no significant influence on cytokine synthesis inhibition. Another protein, PI3K, was also found to phosphorylate Stat3. PI3K inhibition, unlike JAK inhibition, did have a significant impact on cytokine synthesis. The difference between PI3K and JAK in Stat3 phosphorylation is that PI3K phosphorylates Stat3 on the S727 residue whereas JAK phosphorylates Stat3 on the Y705 residue. This difference in phosphorylation positions seems to be the key factor in Stat3 activation leading to inhibition of pro-inflammatory cytokine synthesis. In fact, when a PI3K inhibitor is added to cells, the cytokine synthesis levels are significantly restored. The fact that cytokine levels are not completely restored indicates there is another pathway activated by cmvIL-10 that is inhibiting cytokine system synthesis. The proposed mechanism is that cmvIL-10 activates PI3K which in turn activates PKB (Akt). PKB may then activate mTOR, which may target Stat3 for phosphorylation on the S727 residue. [19]

    MHC downregulation Edit

    Another one of the many ways in which herpes viruses evade the immune system is by down regulation of MHC I and MHC II. This is observed in almost every human herpesvirus. Down regulation of MHC I and MHC II can come about by many different mechanisms, most causing the MHC to be absent from the cell surface. As discussed above, one way is by a viral chemokine homolog such as IL-10. Another mechanism to down regulate MHCs is to encode viral proteins that detain the newly formed MHC in the endoplasmic reticulum (ER). The MHC cannot reach the cell surface and therefore cannot activate the T cell response. The MHCs can also be targeted for destruction in the proteasome or lysosome. The ER protein TAP also plays a role in MHC down regulation. Viral proteins inhibit TAP preventing the MHC from picking up a viral antigen peptide. This prevents proper folding of the MHC and therefore the MHC does not reach the cell surface. [20]

    It is important to note that HLA-G is often up regulated in addition to downregulation of MHC I and MHC II. This prevents the natural killer cell response. [ citation needed ]

    Below are the distinct viruses in this family known to cause disease in humans. [21] [22] [23]

    Human herpesvirus (HHV) classification [1] [22]
    Name Synonym Subfamily Primary Target Cell Syndrome Site of Latency Means of Spread
    HHV‑1 Herpes simplex virus-1 (HSV-1) α (Alpha) Mucoepithelial Oral and/or genital herpes, herpetic gingivostomatitis, pharyngitis, eczema herpeticum, herpetic whitlow, herpes simplex keratitis, erythema multiforme, encephalitis, as well as other herpes simplex infections Neuron Close contact (oral or sexually transmitted infection)
    HHV-2 Herpes simplex virus-2 (HSV-2) α Mucoepithelial Oral and/or genital herpes, herpetic gingivostomatitis, pharyngitis, eczema herpeticum, herpetic whitlow, herpes simplex keratitis, erythema multiforme, Mollaret's meningitis, as well as other herpes simplex infections Neuron Close contact (oral or sexually transmitted infection)
    HHV-3 Varicella zoster virus (VZV) α Mucoepithelial Chickenpox and shingles Neuron Respiratory and close contact (including sexually transmitted infection)
    HHV-4 Epstein–Barr virus (EBV) Lymphocryptovirus γ (Gamma) B cells and epithelial cells Epstein-Barr virus-associated lymphoproliferative diseases, a large group of benign, pre-malignant, and malignant diseases including Epstein-Barr virus-positive reactive lymphoid hyperplasia, severe mosquito bite allergy, Epstein-Barr virus-positive reactive lymphoid hyperplasia, Infectious mononucleosis, Burkitt's lymphoma, Epstein–Barr virus-positive Hodgkin lymphoma, extranodal NK/T cell lymphoma, nasal type, Epstein–Barr virus-associated aggressive NK cell leukemia, CNS lymphoma in AIDS patients, post-transplant lymphoproliferative syndrome (PTLD), nasopharyngeal carcinoma, HIV-associated hairy leukoplakia B cell Close contact, transfusions, tissue transplant, and congenital
    HHV-5 Cytomegalovirus (CMV) β (Beta) Monocytes and epithelial cells Infectious mononucleosis-like syndrome, [24] retinitis Monocyte, and ? Saliva, urine, blood, breast milk
    HHV-6A and 6B Roseolovirus β T cells and ? Sixth disease (roseola infantum or exanthem subitum) T cells and ? Respiratory and close contact?
    HHV-7 β T cells and ? drug-induced hypersensitivity syndrome, encephalopathy, hemiconvulsion-hemiplegia-epilepsy syndrome, hepatitis infection, postinfectious myeloradiculoneuropathy, pityriasis rosea, and the reactivation of HHV-4, leading to "mononucleosis-like illness" T cells and ? ?
    HHV-8 Kaposi's sarcoma-associated herpesvirus
    (KSHV), a type of Rhadinovirus
    γ Lymphocyte and other cells Kaposi's sarcoma, primary effusion lymphoma, some types of multicentric Castleman's disease B cell Close contact (sexual), saliva?

    Zoonotic herpesviruses Edit

    In addition to the herpesviruses considered endemic in humans, some viruses associated primarily with animals may infect humans. These are zoonotic infections:

    Zoonotic herpesviruses
    Species Type Synonym Subfamily Human Pathophysiology
    Macaque monkey CeHV-1 Cercopithecine herpesvirus 1, (monkey B virus) α Very unusual, with only approximately 25 human cases reported. [25] Untreated infection is often deadly sixteen of the 25 cases resulted in fatal encephalomyelitis. At least four cases resulted in survival with severe neurologic impairment. [25] [26] Symptom awareness and early treatment are important for laboratory workers facing exposure. [27]
    Mouse MuHV-4 Murid herpesvirus 68 (MHV-68) γ Zoonotic infection found in 4.5% of general population and more common in laboratory workers handling infected mice. [28] ELISA tests show factor-of-four (x4) false positive results, due to antibody cross-reaction with other herpesviruses. [28]

    In animal virology, the best known herpesviruses belong to the subfamily Alphaherpesvirinae. Research on pseudorabies virus (PrV), the causative agent of Aujeszky's disease in pigs, has pioneered animal disease control with genetically modified vaccines. PrV is now extensively studied as a model for basic processes during lytic herpesvirus infection, and for unraveling molecular mechanisms of herpesvirus neurotropism, whereas bovine herpesvirus 1, the causative agent of bovine infectious rhinotracheitis and pustular vulvovaginitis, is analyzed to elucidate molecular mechanisms of latency. The avian infectious laryngotracheitis virus is phylogenetically distant from these two viruses and serves to underline similarity and diversity within the Alphaherpesvirinae. [2] [3]

    Research is currently ongoing into a variety of side-effect or co-conditions related to the herpesviruses. These include:

    Stages in Adenovirus Life Cycle

    The life cycle of adenovirus can be summarized in the following stages:


    Adenovirus gets attached to the host cell surface by two-stage interactions, namely:

    Initial interaction: In this stage, the attachment of penton fibre occurs with the host cell receptor. A knob of the fibre protein attaches with the CAR family’s cell receptors (Coxsackievirus Adenovirus Receptor). CD46 is the most common receptor for all the serotypes of adenovirus. The host cell also possesses receptors like MHC-I, MHC-II molecules and sialic acid residues.

    Secondary interaction: Attachment of the penton base occurs with the host cell’s αV integrin protein during the secondary interaction or co-receptor interaction.


    There is a special motif in the adenovirus structure called the “Arginine glycine aspartate motif ”. The configuration of the arginine glycine aspartate motif helps an adenovirus to get internalized into the host cell. The process of internalization is very specific or selective. The αV integrin protein gives a signal for the particular serotype of the virus and results in the induction of actin polymerase to uptake the virus.


    It merely refers to the process of adenovirus internalization by the host cell membrane into the cytoplasm. The arginine glycine aspartate motif of the penton base associates with the host cell’s αV integrin protein and results in adenovirus endocytosis. A process of endocytosis or “receptor-mediated endocytosis” occurs through CCPs (Clathrin coated pits) of the host cell membrane.

    Vesicle Formation: When the adenovirus enters the host cell, a vesicle forms around it and called “Endosome”. This is a unique feature, where the whole virus gets into the host cell cytoplasm rather than the genetic material.

    Viral Uncoating

    The virion gets released from the endosome as a result of endosome acidification. The endosome’s acidification results in a dissociation of the protein particles like fibre and capsid into the cytoplasm. Only the viral DNA moves into the host cell’s nucleus for the process of replication and multiplication.

    Replication and Biosynthesis

    The viral DNA replicates inside the nucleus. A 55 KD terminal protein acts as a primer and attaches with each 5’ end of the viral ds-DNA. This terminal protein initiates the synthesis of viral DNA. In adenovirus, two kinds of replication mainly occur:

    The early phase of DNA replication occurs inside the nucleus, which will produce the early genes. The early gene products will undergo transcription to produce early viral mRNA and move to the host cell cytoplasm. A viral mRNA will further undergo translation and produce the early viral regulatory proteins. Early viral protein brings the S-phase of the host cell.

    The late phase of DNA replication occurs inside the nucleus, which will produce the late genes. The late gene products will undergo transcription to produce late viral mRNA in the host cell cytoplasm. A viral mRNA will further undergo translation and form the late viral structural proteins.

    Bioassembly and Release

    After the adenovirus gene expression or the completion of the mRNA translation, all the virion proteins or particles get assembled. The viral DNA is first packaged into the capsid along with penton fibres, and the process called “Maturation”. The mature viral progenies finally leave the host cell either through budding or cell lysis and later infect other cells.


    The adenovirus primarily infects the epithelial cells of the respiratory tract, urinary tract, intestinal tract and lining of the eyes. When it finds a specific host cell, it replicates and undergoes multiplication in the epithelial cells of the conjunctiva, cornea, pharynx etc.

    After infecting the epithelial cells, it can further spread to an infected person’s regional lymph nodes. Usually, an adenovirus infection does not spread beyond the regional lymph nodes but can also affect visceral organs in some cases.

    Host cell and Virus Interaction

    Viral progenies release out of the host cell and mainly produce the following types of infection with the host cell:

    Productive infection

    It is also called “Lytic infection”. Productive infection can define as the type of infection where the viral genome undergoes complete replication and causes cell death by releasing viral progenies. Symptoms start appearing after a few days of infection.

    Abortive infection

    It can define as a form of infection where the viral genome undergoes incomplete replication. Thus, a virus is unable to produce viral progenies in abortive infection, but the infection remains persistent to the host cell.

    Latent infection

    It is a type of infection in which the virus particles remain inside the host cells or tissues. In latent infection, the virus particles persist in a latent or hidden form, but the symptoms appear once the host cell’s immunity or resistance becomes low.

    Oncogenic transformation

    One of the unique features of adenovirus is its oncogenic property. Some serotypes like A and B can transform the host cell into the cancerous cell after viral DNA integration.

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    6 thoughts on &ldquo The Evolution of the Human Life Cycle &rdquo

    The most interesting part of this chapter was reading about the evolutionary implications for changes in life history. It makes sense that any alteration in life history theory would culminate in speciation as the patterns of the growth of youngsters has a huge impact on reproductive strategies. I was particularly interested in the section about menopause since my personal research focus is on gerontological anthropology. I would hypothesize, and hopefully eventually explore, the relationship between a culture's reliance on alloparenting by grandparents and the corresponding length of post-reproductive "healthy years" by each parent. I would also hypothesize that grandmothers with grandchildren from a daughter will be healthier than grandmothers who only bore male children, due to the absence of any parental uncertainty. Would anyone agree (or disagree)?

    What other outside factors can affect a fetus in vivo?

    There are numerous factors, probably more than most pregnant women would like to know, which can affect a fetus in utero. Some of these factors include diet (e.g., nutritious value), air quality (e.g., pollution), stress, how much weight the mother gains or doesn’t gain, and age of the mother. I find studies that examine the factors that can have negative and positive effects on a fetus during pregnancy very interesting. I think this specific avenue of research is very important for informing women of the factors that can play a role in either positively or negatively affecting their growing fetus. Seeing as how diet is the easiest factor for pregnant women to control, I think that is the topic public education should place the most emphasis on. There are so many popular misconceptions that both men and women continue to believe and adhere to, such as pregnant women should eat twice as much food because they are eating for two. Unfortunately for those who believe this misconception, they could end up gaining more weight than is necessary during pregnancy and potentially giving birth to a high weight baby. Although most research has focused on the implications of low birthweights, a recent study has found a positive association between high birthweight (>

    8.8 Ibs) and an increased risk of both childhood and adult malignancies (i.e., malignant tumors) (Ross 2006). My husband I want to start having kids in the next couple of years, so having this type of information is personally very important to me. I have a pretty good general idea of the things I should and should not do or be aware of during pregnancy. However, there are some of factors that I know I won’t be able to control, such as pollution.

    We, unlike other primate species, have an extended period of adolescence. It is our longest life stage before adulthood. This could be because we learn how to maneuver through society during adolescence. Having large, complex social groups requires that humans have a longer time to develop their social skills. Most other mammals that have large social groups go through some sort of juvenile stage, although it does not match human adolescence. Human adolescence is also characterized by skeletal growth spurts, which is interesting because it doesn't happen in any other great ape.

    How would we be different if we had a postnatal period?

    I figure I just missed this part of the reading, but what is meant by postnatal period? I googled and got that it was the same as the postpartum period in women, which we do have.

    -outside factors that can affect a fetus-

    Diet seems like the most obvious factor that could and can affect an unborn baby, this is also the factor that would affect me the most. The risk of mercury or methylmercury poisoning (found in seafood and freshwater fish) could cause great harm to a fetus. Unfortunately I am an avid seafood eater and this will be hard to accommodate if I ever find myself to be with child. The United States food and drug administration advises pregnant women to not eat swordfish, shark, king mackerel or tilefish. Some other factors that can affect a fetus are chemical ones. Alcohol (even a little) can lead to problems with brain development. Mass amount of alcohol can lead to fetal alcohol syndrome. Smoking can also have negative affects on an unborn child and has been known to slow the growth of the fetus. Other factors include lead, dioxins, air pollution and pesticides. Many books and blogs recommend that preggo women stay away from paint supplies, check the quality of their tap water, make sure they aren't living in a home painted with lead paint, wash all produce thoroughly and that they avoid all cleaning products labeled toxic.

    What other outside factors can affect a fetus in vivo?

    There are many factors that can affect a fetus in vivo. There are factors that vary from the environment to the diet of the mother. We have discussed in class before how air pollution in the air quality that the mother inhales during pregnancy can affect the fetus. The diet of the mother is also very important because this strongly influences the development of the baby. For example Fetal Alcohol Syndrome is the conscience of a mother consuming alcohol during pregnancy and the result is the child disfigured and can have mental disabilities as well. This syndrome intrigues me because there is not much known about what causes it. I learned about my freshman year in a biology class so there might be more research that has been conducted on it that I'm unaware of.

    What other outside factors can affect a fetus in vivo?
    Everyone else seems to be answering this question but it affects me personally so I will too! I've heard for ages that drinking alcohol is forbidden during pregnancy, but recently I've been hearing it is OK to have a little bit every now and then during pregnancy. I think because of all the unknown factors, it's still advised against by the CDC etc. but that is definitely something that intrigued me the first time I heard it.
    What physiological changes needed to occur in early human ancestors to accommodate larger brains?
    In addition to larger skulls (duh) there had to be changes to the birth canal and postnatal development. Females' skeletal structure needed to be able to accommodate their big-headed babies when giving birth. And even when these changes occurred, human brains were still too large, so a good bit of development happens in the first few months after birth.
    I'm not sure I understand what you mean by your questions under "Food for Thought."

    Biological life cycle

    A life cycle is a period involving one generation of an organism through means of reproduction, whether through asexual reproduction or sexual reproduction.

    In regard to its ploidy, there are three types of cycles haplontic life cycle, diplontic life cycle, diplobiontic life cycle.

    These three types of cycles feature alternating haploid and diploid phases (n and 2n).

    The haploid organism becomes diploid through fertilization, which joins of gametes.

    This results in a zygote which then germinates.

    To return to a haploid stage, meiosis must occur.

    The cycles differ in the product of meiosis, and whether mitosis (growth) occurs.

    Zygotic and gametic meioses have one mitotic stage and form: during the n phase in zygotic meiosis and during the 2n phase in gametic meiosis.

    Therefore, zygotic and gametic meiosis are collectively term haplobiontic (single mitosis per phase).

    Sporic meiosis, on the other hand, has two mitosis events (diplobiontic): one in each phase.

    Life Cycle of Angiosperms

    Angiosperms, or flowering plants, are the most abundant and diverse plants on Earth.Angiosperms evolved several reproductive adaptations that have contributed to their success. Like all vascular plants, their life cycle is dominated by the sporophyte generation. A typical angiosperm life cycle is shown in Figure below.

    Life cycle of an angiosperm

    The flower in Figure above is obviously an innovation in the angiosperm life cycle. Flowersform on the dominant sporophyte plant. They consist of highly specialized male and female reproductive organs. Flowers produce spores that develop into gametophytes. Male gametophytes consist of just a few cells within a pollen grain and produce sperm. Female gametophytes produce eggs inside the ovaries of flowers. Flowers also attract animalpollinators.

    If pollination and fertilization occur, a diploid zygote forms within an ovule in the ovary. The zygote develops into an embryo inside a seed, which forms from the ovule and also contains food to nourish the embryo. The ovary surrounding the seed may develop into a fruit. Fruitsattract animals that may disperse the seeds they contain. If a seed germinates, it may grow into a mature sporophyte plant and repeat the cycle.

    What is a Haplodiplontic life cycle?

    Adjective. haplodiplontic (not comparable) (biology, of a life cycle) Having multicellular diploid and haploid stages.

    One may also ask, what is life cycle of an organism? A life cycle is defined as the developmental stages that occur during an organism's lifetime. In general, the life cycles of plants and animals have three basic stages including a fertilized egg or seed, immature juvenile, and adult. The time it takes for an organism to complete its life cycle is called a life span.

    Beside this, what is the difference between Haplontic and Diplontic life cycle?

    The main difference between haplontic and diplontic life cycle is that the main form of the haplontic life cycle is haploid and its diploid zygote is formed for a short period of time whereas the main form of the diplontic life cycle is diploid, which produce gametes.

    What is a diploid life cycle?

    Organisms with a diploid life cycle spend the majority of their lives as diploid adults. When they are ready to reproduce, they undergo meiosis and produce haploid gametes. Gametes then unite in fertilization and form a diploid zygote, which immediately enters G1 of the cell cycle. Next, the zygote's DNA is replicated.

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